text:
What could cause spiral tree growth?
While hiking through one of the areas burned in the 1988 Yellowstone fires, I noticed that some of the trees appeared to have grown in spiral patterns.
Most downed trees have crack patterns that imply straight growth, but some look like the one in the picture.  The direction shown in the picture seems to be more common, but it's not universal, and it doesn't appear to be related to location -- another picture I took shows two adjacent logs that spiral in opposite directions.

The two commonly put-forward explanations for spiral growth of tree trunks related to stress-loading and damage-tolerance.
The stress-loading explanation states that spiral-grained trees flex more than straight-grained trees before they break. Flexibility under stress-loading is useful in areas with heavy snowfall (as the tree can flex until the snow falls off) and in areas with heavy wind (as the tree can flex in response to wind-buffeting instead of breaking).
The damage-tolerance explanation states that in trees with straight grain, the leaves (or needles, etc) have water delivered to them, via the xylem, from the roots on the same side of the trunk. In spiral-grained trees with several years of growth, water and nutrients from a given root can be transported to branches on all sides of the trunk. Therefore in spiral-grained trees, if one section of the tree's root system is damaged, it does not necessarily mean that a corresponding part of the canopy will have to die off.
Kubler (1991) discusses both the stress-loading and damage-tolerance explanations in much more detail, if you're interested in further reading.

Is this essentially to imply that trees spontaneously express this growth pattern in response to specific environmental conditions during their development?

From Kubler (1991; linked in answer): "One cannot, however, expect a strict causal relationship between environmental conditions and fiber directions, because spiral grain is "under a considerable degree of genetic control in many species;" only in some species the genetic control of spirality appears to be negligible (Harris 1989, p 159)".
So, mostly no, but some species may develop spirally in response to environmental conditions.

Thanks; sorry, I had just assumed it would be paywalled and didn't even make it to the abstract in this case.


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What type of jellyfish is this
I have been swimming in the seas around Minorca and saw a jellyfish I had not seen before.
I have tried to find it and have (eventually) found 1 single picture of the jellyfish.

The problem I have is, the image is from one of these "buy our picture" website and offers no information about the creature.
What type of Jellyfish is this and can I assume from the picture that it does not actually sting humans?
I have researched, and viewed sites like (As well as Google/Bing images)
http://www.holidays-majorca.co.uk/trips/beaches/types-jellyfish-around-majorca
http://www.seafriends.org.nz/indepth/jellyfish.htm (I know, it's NZ but I'm looking everywhere I can)
http://www.glaucus.org.uk/Moonjell.htm
http://www.whatsthatfish.com/browse/tags/limit/Jellyfish
http://www.imenorca.com/en/entrada-de-blog/jellyfish-minorca
http://www.menorca-tips.com/EN-jellyfish.html
http://www.mcsuk.org/downloads/wildlife/Jellyfishguide.pdf

Same species? Found yesterday on Palm Island, Dubai

https://jellywatch.org/

Eventually, I've stumbled upon an article which calls it a cigar jellyfish.
Further research even shows a very empty entry on Wiki about it, which consists of the single line entry:

The cigar jellyfish (Olindias phosphorica) is a species of jellyfish from the Central and East Atlantic, and the Mediterranean Sea, including off Malta.[2]

Also an interesting article about it being 'rare' in Malta (despite the above information)

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Halophiles' food habit
We know that some halophiles are heterotrophic, but in those highly saline environment what do these organisms eat as there might be very little chance of survival of any other organism?

When we look at the definition, Halophiles are just archaebacteria that require salt in their environment to live. Wikipedia states that they live in salt concentrations of 0.3 to 0.8 M (1.7 to 4.8% — seawater is 0.6 M or 3.5%).
According to The Saltwater Wetland bacteria in estuaries will get their food from dissolved organic mater in the water. An estuary can have a salt concentration of 0.5 to 35 ppt (according to google). This would be 0.05 - 3.5% salinity depending on the estuary, so obviously there are some estuaries would not be able to host Halophiles, but the concept is still the same. They would get their food from dissolved organic matter in the water.

Of course @KritikaWaghmare if it's what you were looking for click the check next to this answer to accept it. If you're looking for more you can wait to see if there are other answers :)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Why are published chromosome counts for polyploids often incorrect by an integer multiplication factor of the original diploid like count?
Why are published chromosome counts (done using techniques such as root smashes) for polyploidy flowering plants often incorrect by a multiplication factor of 2 or 3 from the original diploid like count?
When published chromosome counts for some polyploidy orchid and rhododendron species were updated such counts showed a multiplication of the original more diploid like count rather than a incremental refinement to a slightly more accurate count already in the polyploidy range.
See Ploidy Orchids
In rhododendron multiple counts of 26 chromosomes for R. austrinum, atlanticum, and luteum have been updated indicating a number of chromosomes for these three species is closer to 52 chromosomes.
Is there something about the way a polyploidy flowering plant species undergoes meiosis or mitosis that causes such miscounting to be the chromosome count for closely related diploids?

Your questions do not make sense. Please provide specific examples, i.e. In species x, which chromosomes in that species, etc. The answers will be different based on the organism. Also please use quantifiable terms as a lot and a little are completely subjective. Getting an additional copy of even a part of a chromosome in a human can be lethal during development, others can survive, but lead to dosage dependent conditions. In plants, they can likely sustain polyploidy, but there are probably examples that would be lethal as well.

Also you could provide links to the studies that you are referring to that generated your questions in the first place. If these are unpublished findings then providing the relevant data for others to evaluate the questions would be productive.

@AMR The question now is specific to flowering plants such as orchids and rhododendron.

The question now makes sense, unfortunately I now very little about plant genetics, other than green wrinkled peas and purple or white flowers, etc... Hope someone with knowledge on the subject gets back to you.... My intuition would say however, in your example of 26 to 52, than the plant is completing S phase of mitosis and then stopping, or the cells are multinucleated, sort of like human muscle cells, but again, that is strictly speculation and not based on a knowledge of the subject of the question.


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Are all dipeptides synthesizable?
Probably a basic question, but are all possible dipeptides synthesizable?
For 20 amino acids, there should be in principle 190 dipeptides; do they
all exist or is there chemistry that makes some combinations unstable?
A straight forward generalization would be to ask what percentage of
peptides (or proteins) are synthesizable (in the lab or in cells).

Yes, all dipeptides can be synthesized - it's simply connecting the carboxyl group of the first amino acid to the primary amine of the second amino acid. No big deal. The second part of your question does not make sense - what do you mean? Given a supply of amino acids, a cell can synthesize any protein in its genome. There are limitations of polypeptide synthesis in the lab which increase as the peptide chain grows. There is a large body of literature on this.

I'm pretty sure any peptide can be synthesized in a lab. Length is probably limited by yield, but I imagine that can be overcome by, say, ligating or elongating previously synthesized peptides.

@MattDMo, I'm asking the question without necessarily  referening to genomes or what happens in the cell. As an abstract alphabet of 20 letters you can create a huge number of combinations of words of length N; translating the letters to amino acids and the words to peptides, how many of these words are synthesizable? It seems your answer for N=2 is 100%. For larger N I can't imagine this to be true,  or maybe I'm wrong.

@secretlyfamous You mention cells in your question, which is why I brought them up. In cells, N can be quite large, well over 34,000 in the case of the muscle protein titin. As I mentioned in my previous comment, there is a large body of literature on the capabilities and limitations of chemical polypeptide synthesis, with yield inversely proportional to length. A quick Google search yielded this page, which describes the synthesis of 169 AA by the ligation of several shorter precursors.

@canadianer I highly doubt titin could be synthesized in the lab, though with a good deal of work a lot of (much) smaller proteins probably could. N is not infinite, though. I know antibodies can't be chemically synthesized (two 50 kDa chains and two 25 kDa ones for IgG). Plus, post-translational modifications like disulfide bonds could present a lot of problems.

@secretlyfamous If your interests are entirely in the realm of chemical peptide synthesis, you may find a lot more experience at [chemistry.se] than here. While biochemistry is on-topic here, this question seems to have a lot more chemistry than bio.

@MattDMo, thanks for the clarification. My interest is mainly in the statistics. The actual mechanism is far too complex for me to pursue. I wasn't sure about which tags to use; plus it looks like some of my tags were editted out.

@MattDMo I really don't know anything about it, though I did say peptide and not protein. Is it impossible to synthesize antibodies or just not practical?

Yes. There is nothing magical or mysterious about a peptide bond.

@canadianer Yields drop off very quickly above 20 - 30 amino acids, with bad products making up more of the mix. Disulfides are a pain, but there are ways to control them using protecting groups. The nice thing about peptide synthesis is being able to use a huge variety of amino acids, which has allowed some neat stuff.

I see no reason why not. Just to make sure, I decided to test. I ran a search on all human proteins (using the UniProt flat file) for all possible dipeptide combinations of the 20 standard amino acids (selenocysteine is also present in humans but only in 22--or so, depending on how you count them--proteins, so I wouldn't expect all possible sec-containing dipeptides to be present) .
As expected, each of the 400 possible dipeptides were indeed present in at least one human protein. In case anyone wants to repeat this, the "protocol" is as follows:

Download the human flat file from Expassy.
Extract the peptide sequences
perl -ne 'if(s/^\s+//){s/\s+//g;print}' human.flat > human.pep

Generate the list of possible dipeptides:
AA
AC
AD
AE
AF
AG
AH
AI
AK
AL
AM
AN
AP
AQ
AR
AS
AT
AV
AW
AY
CA
CC
CD
CE
CF
CG
CH
CI
CK
CL
CM
CN
CP
CQ
CR
CS
CT
CV
CW
CY
DA
DC
DD
DE
DF
DG
DH
DI
DK
DL
DM
DN
DP
DQ
DR
DS
DT
DV
DW
DY
EA
EC
ED
EE
EF
EG
EH
EI
EK
EL
EM
EN
EP
EQ
ER
ES
ET
EV
EW
EY
FA
FC
FD
FE
FF
FG
FH
FI
FK
FL
FM
FN
FP
FQ
FR
FS
FT
FV
FW
FY
GA
GC
GD
GE
GF
GG
GH
GI
GK
GL
GM
GN
GP
GQ
GR
GS
GT
GV
GW
GY
HA
HC
HD
HE
HF
HG
HH
HI
HK
HL
HM
HN
HP
HQ
HR
HS
HT
HV
HW
HY
IA
IC
ID
IE
IF
IG
IH
II
IK
IL
IM
IN
IP
IQ
IR
IS
IT
IV
IW
IY
KA
KC
KD
KE
KF
KG
KH
KI
KK
KL
KM
KN
KP
KQ
KR
KS
KT
KV
KW
KY
LA
LC
LD
LE
LF
LG
LH
LI
LK
LL
LM
LN
LP
LQ
LR
LS
LT
LV
LW
LY
MA
MC
MD
ME
MF
MG
MH
MI
MK
ML
MM
MN
MP
MQ
MR
MS
MT
MV
MW
MY
NA
NC
ND
NE
NF
NG
NH
NI
NK
NL
NM
NN
NP
NQ
NR
NS
NT
NV
NW
NY
PA
PC
PD
PE
PF
PG
PH
PI
PK
PL
PM
PN
PP
PQ
PR
PS
PT
PV
PW
PY
QA
QC
QD
QE
QF
QG
QH
QI
QK
QL
QM
QN
QP
QQ
QR
QS
QT
QV
QW
QY
RA
RC
RD
RE
RF
RG
RH
RI
RK
RL
RM
RN
RP
RQ
RR
RS
RT
RV
RW
RY
SA
SC
SD
SE
SF
SG
SH
SI
SK
SL
SM
SN
SP
SQ
SR
SS
ST
SV
SW
SY
TA
TC
TD
TE
TF
TG
TH
TI
TK
TL
TM
TN
TP
TQ
TR
TS
TT
TV
TW
TY
VA
VC
VD
VE
VF
VG
VH
VI
VK
VL
VM
VN
VP
VQ
VR
VS
VT
VV
VW
VY
WA
WC
WD
WE
WF
WG
WH
WI
WK
WL
WM
WN
WP
WQ
WR
WS
WT
WV
WW
WY
YA
YC
YD
YE
YF
YG
YH
YI
YK
YL
YM
YN
YP
YQ
YR
YS
YT
YV
YW
YY

Save that list as dip.txt.
Use that file to search the protein sequences:
perl -ne 'BEGIN{open(A,"human.pep"); while(<A>){chomp; $k.=$_}}; chomp; print "$_\n" if $k=~/$_/  ' dip.txt

The script above will print each dipeptide that was found in at least one protein. Since all were printed, all dipeptides exist in the human proteome.

thanks for the detailed answer. Your answer looks at things from a slightly
different angle (dipeptide occurrence in proteins) which is actually a more interesting
angle. I asked a simplified question about dipeptide occurrence on their own first;
the answer to that seems to be yes. I am also in fact interested in the case for larger
N and the statistics of their occurrence in proteins. I'll take a shot at modifying your
script to do some more searches. BTW, you caught a mistake in the number of possible
combinations of dipeptides, it is in fact 400 and not 190 as I put in the question.

Yeah, a negative result wouldn't have been conclusive but a positive one is. My assumption was that if a dipeptide occurs in a protein, it can be synthesized. You seem to be suggesting that the dipeptide alone might not be stable and could need the rest of the peptide in order to be so. That's quite interesting and may well be the case but my structural chemistry knowledge is pitiful so I won't venture an opinion on it. As for larger Ns, my script won't help you much. It's a very simplistic approach.


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What makes tones sufficiently useful that it would lead to the evolution of tonal processing?
I will define a "tone" as  a steady periodic sound. As an example, I consider a sinusoidal wave to be a tone. By "tonal processing", I mean ratio relationships between the notes. For instance, if I play 220Hz sine wave then a 440Hz wave will be perceived as an octave higher.
I don't understand why humans have the ability to perceive frequency relationships between tones. I have read several evolutionary anthropology books like The Singing Neanderthal and Finding Our Tongues and, between these two books, they suggest that the obvious evolutionary purpose of music is for communication. Each author takes a slightly different approach but the basic underlying point remains that tonal processing exists because it gives us advantageous communication abilities. But even accepting this hypothesis, it doesn't explain why humans have a tonal processing mechanism that is specific enough to perceive ratio differences between notes. The tonotopic organization of both the basilar membrane and the precortical auditory pathways might partially account for the machinery used for tonal processing and why the advanced forms in music could have developed. But this still leaves us with the question as to why would such information be useful?
I remember reading somewhere one person hypothesized that the purpose of perceiving these differences was to identify "relative pitch", i.e. the ability to identify or re-create a given musical note by comparing it to a reference note and identifying the interval between those two notes. But this hypothesis doesn't really make complete sense to me because it doesn't explain why the brin can have such specificity when identifying the ratio between two notes.
Another phenomena that seems pertinent is the idea of a "drifting reference point" which Glimcher discusses in Foundations of Neuroeconomic  Analysis. In Chapter 12, he explains how our perception of color isn't fixed but depends on context and in this sense drifts. IIRC, there is a literature that discusses possible neural mechanisms for this. Perhaps something similar would be relevant here for explaining why humans can process tones so precisely.
My Question:
What are the accepted arguments for why would ratios between tones would be be useful information for social communication?
Just to clarify, I am expecting the answer to this question to involve a discussion of the physical properties of tones and why a hominid brain would find this useful information for communication purposes.

I don't understand the question. Is it "why can we process multiple frequencies" or "why do we appreciate music". If the former, then you have to realize that not only music contains various frequencies, but e.g. speech contains a range of frequencies as well.

I think the whole issue is that you put all your focus into music. The ability to tell apart different tones hasn't evolved with the culture of music playing. It is much older.
Ability to distinguish different tones in non-human animals
Humans are of course not the only animals that are able to recognize tones. Mice for example can as well accurately tell the difference between two close tones (ref.).
Perceiving its environment
So why is the ability to tell different tones apart important. It is important because it allows one organism to better perceive the elements in its surrounding. For example, consider being in the savanna and you can't tell the difference between a lion roaring and a water fall. It seems to be a pretty important handicap.
Tones recognition in social contexts
A very large part of animal's communication is based on tons. Very primitive forms of language are mostly based on tones. Courtship display for example is often based on the tone of the other gender (the tone is correlated with the size of the organ producing the tone). A very large part of human's communication is based on tone as well. You might want to have a look at Albert Mehrabian.
If you have more questions about the importance of non-verbal communication you will need to ask your questions to psychologists (on CognitiveScience.SE) and not to biologists. Note btw, that the condition of being unable of recognizing different tones is called tone deafness.

+1 Interesting. I didn't realize mice could perceive differences between tones.

In short, I suspect that the answer is not so much that it is useful to recognize tonal relationships, but that it is easy.
It sounds like why or how we can distinguish pitch at all is a separate question which you have already accepted. So let's take as a given that whatever purpose our hearing serves, what we have ended up with is machinery which can usually tell higher tones from lower tones.
Now, it turns out that this by itself is not a simple problem to solve. Real, natural sound is never a simple sinusoidal wave. If you hear a pure sinusoidal wave played over a speaker, it sounds synthetic, like maybe a pitch fork, a singing bowl, or a computer - definitely something man-made. That's because absolutely nothing natural makes a sound like that. Consider any natural thing that for even a moment holds a single tone, like a long tone from within birdsong, or the long tone at the peak of a wolf's howl, or wind whistling through a cavern. If you heard samples of each at exactly the same pitch, they would still be distinguishable, just as a clarinet is distinguishable from a flute, or in fact, to the trained ear, two clarinets are distinguishable from one another. This is because the wave that reaches your ear is actually much more complex than a simple sine wave.
In fact, if you saw the high-fidelity digital wave representation of almost any sound which we would consider to be a single tone of one steady pitch, you might have a lot of trouble identifying the period of that wave (which correlates to it's pitch). In digital processing, to identify the tone in a digital wave, or for that matter, the many tones represented in a piece of music, we run a complicated calculation on the wave called a Fourier Transform.
Our aural machinery came up with a fascinating solution to the problem of distinguishing frequencies. Rather than discovering the mathematical method for calculating a "Fast Fourier Transform", our inner ears contain thousands of stereocilia - little hairs of varying lengths which vibrate at different frequencies. Rather than trying to determine the periodicity of a wave by any sort of analysis, these hairs automatically vibrate when any frequency within the wave resonates precisely with their length. This allows us to hear the various frequencies within the sound wave that reaches our ear, so that we can take in the whole ensemble of our environment.
Now here's the catch. A hair that vibrates at exactly 440Hz, also vibrates pretty well at 220Hz. In a sense, this actually represents a weakness in our hearing strategy. Even though the one frequency is twice as fast as the other, they actually sound a lot alike to us. It is harder for us to distinguish middle C (C4) from the C an octave above (C5) than it is for us to distinguish middle C from the D-flat right above it. We can still recognize the difference, but when we do, part of what we recognize is their likeness. Other intervals share the same characteristic in different ways. For example, double a frequency is one octave higher, but three times that same frequency is a fifth above that.
So, from an evolutionary perspective, this is a coincidence of the handy solution found to distinguish tones. However, the joy we find in music is so serendipitous as to beg for a more divine explanation, which you will find echoed throughout our history and surely our future, and within any moment in which you find yourself appreciating the beauty of well-tempered harmony.

This was really interesting! Thanks very much. A bunch of things you mentioned I knew already but you helped me fit them together very nicely. Like I hadn't completely gotten what Fourier transforms were used for. Thx :D

As I understand it, Fourier Transforms are used in the breakdown and analysis of all kinds of signals. But I personally had the opportunity in school to see how they operate on the vibration of a single guitar string. G, I think it was. The transform breaks down the wave (which is a function of point intensity over time) into a display of frequency intensity (where frequency is on the X axis and cumulative intensity is on Y). I was fascinated to see that although the correct frequency for that G was the strongest frequency present, numerous other undertones and harmonics were in the signal.


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Can bigger persons generally resist g-forces better?
I've seen a claim that bigger persons generally resist g-forces worse than smaller in an undergraduate biology book. However this claim was supported by the argument that blood has to travel a longer way form the head to the heart.
However, I think this is not the only factor that matters. They generally should have a larger heart, but may need to pump more blood, so perhaps this cancels.
Questions:

Has it ever been tested whether bigger persons generally resist g-forces better? If so, what were the results?
If we only take scale factors in considerations, i.e. we take identical persons, but the one is 1.2 times as large as the other in all dimensions, what conclusion will we reach? What factors should we take into consideration?

You also need to include factors like Muscle/Fat ratios. Like you wouldn't wanna test a small athletic person against an overweight giant,

Has ever what been tested? And which scale factors?

@AliceD I have tried to clarify the question.

There are some good points on high G-forces in this discussion of launch-abort systems [http://space.stackexchange.com/questions/8155/how-hard-is-it-on-the-crew-to-go-through-the-14-gs-of-a-launchpad-abort-of-the]. It is safe to say that within the size range of adult humans, the size of the person is not a very important concern compared to which way (s)he is facing.
In general, though, larger-scaled things fail under lesser forces than smaller-scaled things because strength increases as a square function of linear measurements, whereas masses increase as a cubic function.

What is "g-forces"?? Can you please use standard terminology?

@WYSIWYG G-forces. Feel free to edit the question to add in a more biological correct term.

@wythagoras I don't think the term "g-force" is used in any scientific literature. I am not sure if I am getting too old for this but I have always seen and used "Gravitational force" or "acceleration due to gravity" in such contexts.


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What is "chain identifier" in PDB?
The PDB file format is explained here. My question is what "chain identifier" is exactly? What is the difference between two residues which have the same sequence number but different chain identifiers?

The "chain identifier" does exactly what it says: it identifies the polypeptide or other molecular chain. For some structures, there is only one, so you'll only see an identifier A. However, many structures show two or more proteins bound together, or an enzyme complexed to a substrate, or a small molecule inhibitor in a binding pocket - there are many different possibilities. Each individual chain of atoms has its own identifier.
For example, 1VKX shows my favorite transcription factor NF-κB bound to the κB DNA enhancer sequence. There are four chains in the structure: two polypeptide chains, the p65 subunit A and the p50 subunit B, and two DNA chains C and D, one for each strand (forward and reverse).


text:
What kind of larvae are these?
My uncle was helping us spray the garage for ants, and he stumbled across a huge batch of some type of larvae. According to him...

"It looked like a long, narrow clump of mud. When I broke it open, all of these larvae fell out. Whatever bugs were inside scattered pretty quickly!"

Geography: We're in Los Angeles, CA (southwestern USA)
Season: It's late summer here (early September)

Exhibit A: The pile of larvae...

Exhibit B: A similar husk of "mud" found in our garage. When it was shattered, nothing fell out...

My uncle thinks it's termites... I'm certainly hoping it isn't.

Not a bug guy, but it does look like termites.

Sorry, but its termite larvae.

I think that it is termites larvae. For more info check this :  Termites follow the typical life cycle of insects that have a gradual life cycle: they begin as eggs, and then enter nymphal to adult stages. In termite development, newly hatched termites are sometimes referred to as “larvae,” which is not to be confused with the larvae of complete metamorphosis insects like flies.
Termite larvae typically hatch within a few weeks. They are approximately the same size as the eggs from which they hatched and are immediately tended to by worker termites. They often comprise a large part of a termite colony.
Similar to other insect young, termite larvae go through a series of molts, during which they shed their skins. From the larval stage, termite larvae may evolve into other members of the colony’s castes.
If you suspect you have termite activity in or near your home, contact a pest control professional. Termite damage can go undetected and result in significant financial loss from their damage. A termite inspector can inspect a home for signs of activity and conditions that are attractive to termites. They also can offer services to treat and protect the home from potential future damage.

Bummer... certainly not what I wanted to hear, but seems to be the consensus. Thanks!

UPDATE: Inspector came today and said "yep, you've got subterranean termites"... so it's officially official.


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What is the significance in an alpha-helix being right-handed or left-handed?
Why is that often when alpha-helices are discussed, it is also mentioned their direction - right-handed (clockwise) or left-handed (anti-clockwise)?
I have heard that left-handed alpha-helices are usually less stable, but I'm sure there is more to it than that?

A quick search sent me here: https://www.quora.com/Why-are-most-alpha-helices-in-proteins-right-handed .

Some experimental and modelling observations suggests, folding energy for right handed in more favorable. You can find more detailed answer to this question here.


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Equilibrium and Metabolism: Can cells exist at STATIC equilibrium? What about dynamic equilibrium?
I understand that in closed systems, once reactions reach equilibrium, they can no longer be used to power other reactions. If a cell was a closed system (which it is not), being at equilibrium would mean that it's dead, for it needs a continuous input of energy from the environment.
I know that the cells are open systems, and my teacher mentions that cells can never be at equilibrium. But, I am confused because can't cells be at dynamic equilibrium (where rates of reactions = rates of products)? So my next question is: can the cells not exist at static equilibrium? I am not quite understanding the differences between equilibrium, dynamic, and static. And, when something is at dynamic equilibrium, why does this mean that the concentrations of reactants and products are not necessarily equal?

There are some things that should be addressed first.

Chemical-Equilibrium
This is a condition at which the forward reaction rate is equal to the backward reaction rate for a reversible reaction.
$$\ce{A<=>[k_f][k_r]B}$$
In this case, $k_f.A=k_r.B$, at the equilibrium, if the reactions are first-order. If $k_f>k_r$, then the concentration of B would be higher than the concentration of A, at equilibrium point.

Steady-State
It is a state of the system at which the overall concentration of all the components (reactants and products) remain constant with time, or oscillate at a constant amplitude and frequency. Mathematically, the differential equations that denote the system (as mentioned by Dexter) would equate to zero.
If this condition applies only for one or more but not all the components of the system, then it is said to be in a Quasi-Steady-State.
If there are only two species which inter-convert but do not get formed or degraded, then steady state would be same as the chemical equilibrium. However, it is to be noted that chemical-equilibrium is a property of a reversible reaction whereas steady state is the property of the system.

Coming to your main question, I do not know what your teacher really had in mind, but this is my explanation.
According to the above definitions, you cannot say that the cell is in equilibrium because the cell is a system and not a reaction. The usage of the term "equilibrium" varies between different fields of study and physicists do use steady-state and equilibrium interchangeably. However, this is not the practice among chemists and biochemists.
Having said that, I would say that a cell does attain a steady state. I think what your teacher wanted to imply was that a cell constantly responds to the external stimuli (which is randomly changing) and therefore never remains at any given steady state for a long time.

Can the cells not exist at static equilibrium?

No, they don't. In fact the term "static equilibrium" in never used in chemistry because it never really happens. At a static equilibrium all the rates have to be zero, whereas in a dynamic equilibrium the rates have to balance each other out. Static equilibrium usually applies only for macroscopic objects (which do not include molecules).
A note on stochasticity: Chemical reactions follow probabilistic kinetics i.e. the reactions occur with some probabilities, instead of fixed rates (these probabilities can be unequal for different reactions). Chemical systems can be approximated by deterministic models at the thermodynamic-limit which reflects the "average" behaviour of the system.

when something is at dynamic equilibrium, why does this mean that the
concentrations of reactants and products are not necessarily equal?

See the first section. Similar logic applies for steady-state. The steady state concentrations depend on the kinetic parameters.

If a cell was a closed system (which it is not),

Yes, you are right. Cell is not closed system.

my teacher mentions that cells can never be at equilibrium

No. It depends on your definition of equilibrium and which kind of equilibrium. E.g.: Cellular membranes are most of the time in chemical equilibrium to maintain their resting potential.

can't cells be at dynamic equilibrium (where rates of reactions = rates of products)?

Yes. Most of cellular processes are assumed to be in dynamic equilibrium which is correct in most of macroscopic phenomenons. Microscopically, everything is stochastic.
Most of cellular processes are assumed to be in dynamic equilibrium.

I am not quite understanding the differences between equilibrium, dynamic, and static. And, when something is at dynamic equilibrium

Look here!

And, when something is at dynamic equilibrium, why does this mean that the concentrations of reactants and products are not necessarily equal?

Suppose system A -> B -> C -> A, with reaction rates v1, v2 and v3. If you write differential equations for this system,
$$
\frac{dA}{dt} = v3\times C - v1\times A\\
\frac{dB}{dt} = v1\times A - v2\times B\\
\frac{dC}{dt} = v2\times B - v3\times C
$$
Now at equilibrium,
$$
v3\times C = v1\times A = v2\times B
$$
Now you can put your v1,v2 and v3 in such way that concentrations of A, B, C will be different. In this care system can be in dynamic equilibrium even when concentrations of A, B and C are not same.

The condition that you are referring to, is specifically called the steady state in chemical and biochemical texts because chemical equilibrium is a different phenomenon. Physicists, generally use the term "equilibrium" to mean steady state.

This is better than all of our mathematical explanations. !

The video is nice.. But I think there are field specific differences (which are quite subtle).


text:
Properties that can be derived from amino acid sequences
What are the properties that can be derived from an amino acid sequence apart from those mentioned in the website? In the mentioned website, the properties that can be calculated from amino acid sequence are:
 1. Molecular weight of protein
 2. Number of amino acids in the protein sequnece
 3. Composition of charged residues (DEKHR)
 4. Composition of aliphatic residues (ILV)
 5. Composition of Aromatic residues (FHWY)
 6. Composition of Polar residues (DERKQN)
 7. Composition of Neutral residues (AGHPSTY)
 8. Composition of Hydrophobic residues (CVLIMFW)
 9. Composition of Positive charged residues (HKR)
10. Composition of Negative charged residues (DE)
11. Composition of tiny residues (ACDGST)
12. Composition of Small residues (EHILKMNPQV)
13. Composition of Large residues (FRWY)

Other than the first two, the rest of the groups seems like a list of binary sets based on specific chemical properties of the amino acids. Without any additional information, this question is too broad.

what additional information do you want. please tell me. Dont just close it. I need this question open.

What exactly do you define as a "property"? The current list is not well defined, and arguably silly examples like "Composition of residues with "E" in their name" are also "properties".

This approach (that you linked to), wherein one takes a purified protein and subjects it to amino acid analysis (or amino acid composition), dates back to a period in time from ~ 1960-1980.  Once molecular cloning was developed it became much faster to clone the gene for a protein to determine its identify rather than sequence the polypeptide itself. Around the same time a gas-phase chromatography device was coupled to a mass spectrometer and marketed commercially by Applied Biosystems, permitting so-called microsequencing of peptide fragments. BLAST is going to be way more sensitive.

Sensitive as in?

Just look at NCBI , EMBL and DDJB tools. These three are premier and global database centres. Their tools are self explanatory. You can calculate lot of things from these sequences. Besides these there are many in house tools for calculating specific information from sequences from many bioinformatics research labs across the world.

Using a helical wheel projection you can make predictions of regions that are likely to form, or adopt, amphipathic helices. These are alpha-helices where one face, or side, of the helix  is largely polar while the opposite, side, or face, of the helix is largely non-polar.
Also, based on known X-Ray crystal structures, there are some residues that are known as helix breakers, like Pro and Gly, and there are other residues that are often found in beta sheets, so you can make secondary structure predictions, based on the primary amino acid sequence.
However, in the absence of extended regions of amino acid sequence identity, these predictions are just hypotheses.

No, i don't want to predict anything, i want confirmed properties, not predictions

Good luck with that.


text:
Plot coverage per base for BAM file
I have a BAM file and a BED file for my own chromosome. I would like to get coverage per base and ideally construct a histogram of coverage across each gene.
The motivation is to visualise the coverage across each gene. If my experiment is good, I should expect uniform coverage. It's also important to compare the coverage near the boundary of the genes.
A R (bioconductor) solution is ideal, because I can directly visualise.
How to do it?

From your bam-file, you can generate a BED(-graph) of per base coverage with bedtools genomecov (use the -ibam, -d and if you want a BEDgraph also the -bg flags).
There are multiple R packages for bioconductor which read and visualise these, including sushi.

skymningen's suggestion of genomecov is absolutely correct. The command I use is:
bedtools genomecov -bg -ibam sorted.bam > sorted.wgx

This generates a BedGraph file.
Unfortunately, the R package sushi had a bug that it didn't generate anything if the interval I wanted is too small. I preferred IGV.


text:
What determines excrement's caliber?
Often, pieces of feces have a clearly-defined shape and size — both length and width (that is, cross-sectional diameter, or caliber). But that width seems to vary quite a bit, even among pieces of feces from the same person. Why? What determines the width? Why is it wide when it's wide, and why is it narrow when it's narrow?

With the help of Bristol Stool Chart (BSC) and full explanation of conditions related to different stool sizes from this link you could have a full understanding over stool size.

» Type 1: Separate hard lumps, like nuts Typical for acute
  disbacteriosis. These stools lack a normal amorphous quality, because
  bacteria are missing and there is nothing to retain water. The lumps
  are hard and abrasive, the typical diameter ranges from 1 to 2 cm
  (0.4–0.8”), and they're painful to pass, because the lumps are hard
  and scratchy. There is a high likelihood of anorectal bleeding from
  mechanical laceration of the anal canal. Typical for post-antibiotic
  treatments and for people attempting fiber-free (low-carb) diets.
  Flatulence isn't likely, because fermentation of fiber isn't taking
  place.
» Type 2: Sausage-like but lumpy Represents a combination of Type 1
  stools impacted into a single mass and lumped together by fiber
  components and some bacteria. Typical for organic constipation. The
  diameter is 3 to 4 cm (1.2–1.6”). This type is the most destructive by
  far because its size is near or exceeds the maximum opening of the
  anal canal‘s aperture (3.5 cm). It‘s bound to cause extreme straining
  during elimination, and most likely to cause anal canal laceration,
  hemorrhoidal prolapse, or diverticulosis. To attain this form, the
  stools must be in the colon for at least several weeks instead of the
  normal 72 hours. Anorectal pain, hemorrhoidal disease, anal fissures,
  withholding or delaying of defecation, and a history of chronic
  constipation are the most likely causes. Minor flatulence is probable.
  A person experiencing these stools is most likely to suffer from
  irritable bowel syndrome because of continuous pressure of large
  stools on the intestinal walls. The possibility of obstruction of the
  small intestine is high, because the large intestine is filled to
  capacity with stools. Adding supplemental fiber to expel these stools
  is dangerous, because the expanded fiber has no place to go, and may
  cause hernia, obstruction, or perforation of the small and large
  intestine alike.
» Type 3: Like a sausage but with cracks in the surface This form has
  all of the characteristics of Type 2 stools, but the transit time is
  faster, between one and two weeks. Typical for latent constipation.
  The diameter is 2 to 3.5 cm (0.8–1.4”). Irritable bowel syndrome is
  likely. Flatulence is minor, because of disbacteriosis. The fact that
  it hasn't became as enlarged as Type 2 suggests that the defecations
  are regular. Straining is required. All of the adverse effects typical
  for Type 2 stools are likely for type 3, especially the rapid
  deterioration of hemorrhoidal disease.
» Type 4: Like a sausage or snake, smooth and soft This form is normal
  for someone defecating once daily. The diameter is 1 to 2 cm
  (0.4–0.8”). The larger diameter suggests a longer transit time or a
  large amount of dietary fiber in the diet.
» Type 5: Soft blobs with clear-cut edges I consider this form ideal.
  It is typical for a person who has stools twice or three times daily,
  after major meals. The diameter is 1 to 1.5 cm (0.4–0.6”).
» Type 6: Fluffy pieces with ragged edges, a mushy stool This form is
  close to the margins of comfort in several respects. First, it may be
  difficult to control the urge, especially when you don‘t have
  immediate access to a bathroom. Second, it is a rather messy affair to
  manage with toilet paper alone, unless you have access to a flexible
  shower or bidet. Otherwise, I consider it borderline normal. These
  kind of stools may suggest a slightly hyperactive colon (fast
  motility), excess dietary potassium, or sudden dehydration or spike in
  blood pressure related to stress (both cause the rapid release of
  water and potassium from blood plasma into the intestinal cavity). It
  can also indicate a hypersensitive personality prone to stress, too
  many spices, drinking water with a high mineral content, or the use of
  osmotic (mineral salts) laxatives.
» Type 7: Watery, no solid pieces This, of course, is diarrhea, a
  subject outside the scope of this chapter with just one important and
  notable exception—so-called paradoxical diarrhea. It‘s typical for
  people (especially young children and infirm or convalescing adults)
  affected by fecal impaction—a condition that follows or accompanies
  type 1 stools. During paradoxical diarrhea the liquid contents of the
  small intestine (up to 1.5–2 liters/quarts daily) have no place to go
  but down, because the large intestine is stuffed with impacted stools
  throughout its entire length. Some water gets absorbed, the rest
  accumulates in the rectum. The reason this type of diarrhea is called
  paradoxical is not because its nature isn‘t known or understood, but
  because being severely constipated and experiencing diarrhea all at
  once, is, indeed, a paradoxical situation. Unfortunately, it‘s all too
  common.
Interestingly, the interpretations and explanations of the BSF scale
  that accompany the original chart differ from my analysis. To this I
  can only say: thanks for great pictures, but, no thanks for the
  rest...
Excerpted from Fiber Menace, page 117-120; BSF Chart: wikipedia.org

But to make it more clear:
Reasons behind thicker and harder stool:

Lower fiber food
Lower liquid intake
Lower physical activity
Lack or lower amount of bacteria related to retaining water inside rectum and colon
Medication:

Many medications have constipation as a side effect. Some include (but
  are not limited to) opioids also known as narcotics, diuretics,
  antidepressants, antihistamines, antispasmodics, anticonvulsants, and
  aluminum antacids. Certain calcium channel blockers such as nifedipine
  and verapamil can cause severe constipation due to dysfunction of
  motility in the rectosigmoid colon.

Metabolic and muscular

Metabolic and endocrine problems which may lead to constipation
  include: hypercalcemia, hypothyroidism, diabetes mellitus, cystic
  fibrosis, and celiac disease. Constipation is also common in
  individuals with muscular and myotonic dystrophy.

Structural and functional abnormalities
Any physical digestive tract line problem which cause interference of stool movement. Like cancer or some kind of inflammation that could ban the canal

Constipation has a number of structural (mechanical, morphological,
  anatomical) causes, including: spinal cord lesions, Parkinson, colon
  cancer, anal fissures, proctitis, and pelvic floor dysfunction.
Constipation also has functional (neurological) causes, including anismus, descending perineum syndrome, and Hirschsprung's disease. In
  infants, Hirschsprung's disease is the most common medical disorder
  associated with constipation. Anismus occurs in a small minority of
  persons with chronic constipation or obstructed defecation.

Psychological

Voluntary withholding of the stool is a common cause of
  constipation.The choice to withhold can be due to factors such as fear
  of pain, fear of public restrooms, or laziness. When a child holds in
  the stool a combination of encouragement, fluids, fiber, and laxatives
  may be useful to overcome the problem.

Edit:
In the second provided link you could get how cross-sectional diameter changes based on what you eat or how you behave with your body mentally or physically if you are a healthy person.
But as you are interested more on cross-sectional size of stool and reason behind it, consider the fact that colons and rectum are water absorber. The more stool stays there the more thick and dry it gets. So if you ate more fiber you will probably have softer stool and thinner caliber as the result of pressure of the rectum canal. Because some bacteria which are active in the fibers of stool are water absorbers too and the reason behind why doctors insist on eating more probiotic products is to keep these bacteria present and stable and also to get vitamins from their activities. So you could change your caliber only by eating more fiber more water and having more physical activities and also for consistent thick and dry stool (constipation) individual must share the problem with doctor because it could bring more dangerous problems in future or maybe it's a sign of some other serious disease that person's body is already dealing with. Most of the time it's nothing but our diet and hours we are sitting for variety of reasons or maybe focusing on another activitys (work, computer games, disabilities, watching tv and so on and so forth).
https://en.wikipedia.org/wiki/Constipation
https://www.gutsense.org/constipation/normal_stools.html

As this post isn't about cross-sectional diameter, it doesn't seem to answer the question.

I've edited my answer to make it more clear to get your answer about why stool size differs even in one person. If there is still something not understandable, feel free to ask. It helps me too.


text:
Can someone die from pain?
I'm a CNA and I just got home from a very long day at work. I just started this job and I got hurt at work last night which made me wonder can enough pain cause death (without suicide)?
I think the answer is yes, but I'd like to know how/why.

Yes, you can go into shock from bleeding, emotional disturbance, a heart disorder, and/or a blood infection. It causes not enough oxygenated blood to get to important organs in your body and if it isn't treated it's normally fatal.
I would think that enough pain could cause a large emotional disturbance which could result in shock.

Please give some solid references. I do think this would be possible though, especially if one has a weak heart; as an increased heart rate from pain could stress it.

Pain and shock are completely different things. Your answer needs references and clarification.


text:
Can a brown recluse bite lead to diabetes?
Ok, I realize that this question may seem crazy at first glance. I would agree. Also, this does deal with a medical diagnosis, however, as I'm more concerned with the explanation behind it, I figured it fit in this category the best. Feel free to move this question (or suggest a better bit) if this is incorrect. On to the question...
Apparently (according to a friend of mine) this person woke up in the morning, could barely move, had a bite-like sore/mark and went to the hospital. Doctor said it was a brown recluse bite and as a result of the incident, this person now has Type 1 diabetes.
It really doesn't matter how (the result is still living with diabetes), but I'm fascinated by this incident and, being neither an expert on spider nor diabetes, I would like to know if this is plausible and, if so, how?
I realize that (1) approximately 80% of brown recluse bites are misdiagnosed and (2) I will never have access to their medical records, but let's operate under the assumption that this was as reported.
From what I've been able to find, in very rare cases, brown recluse venom can result in viscerocutaneous lexoscelism, which may lead to acute kidney failure... but through my research, I can't seem to link that to diabetes (the converse is easy, as diabetes is one of the leading causes of kidney failure).

What (if anything) am I missing?
Is there another response to Lexosceles toxin that can lead to diabetes?
If this isn't possible, what could be an explanation that would cause diabetes but look like a brown recluse bite to a doctor?

This may be better suited for skeptics SE. Wild speculation: antibodies against spider venom are cross reactive.

Hmm...I was debating between the two, however, this seems like a more focused community, with more activity. I've added it to that SE too. Forgive me for my lack of biology knowledge (I'm a physics/CS guy), but what do you mean by "cross reactive"?

@canadianer I think it's better here though, because I wasn't able to find anything on google to support it, so it would be more of a question for a biologist/researcher.... just imo.

https://en.m.wikipedia.org/wiki/Cross-reactivity … https://en.m.wikipedia.org/wiki/Molecular_mimicry

Islet beta cells were shown to undergo apoptosis in a sphingomyelinase-dependent manner in the presence of amyloid peptides like IAPP, article here. Looks interesting, but I'm no expert! Would anyone like to weigh in?

As I am uncertain what type of spider bite my daughter had for sure there were 3 spider bites on her rear while sleeping. As a result of these bites taking a toll on her system she later developed type 1 diabetes. She was 1 1/2 when she was bitten and now 15 living with this terrible disease all behind a spider munching on her. I say that because she had 3 bites in total all of which were filled with puss and have left scars in the effected areas. So yes venom from a spider bite CAN and DOES lead to type 1 diabetes, my baby is a living testimony to that fact. I would so love for someone to fin


text:
What is difference between several mRNA RefSeq for one gene?
I'm looking for mRNA RefSeq sequences for a given gene in the UCSC genome browser by searching gene name "HLA-F" in human (scroll to Refseq genes section). There are several RefSeq mRNA for the gene, what is difference between these RefSeq sequences and which one of them is what I want?

I'll walk you through the process of determining this:

Note that there are two gene names presented: HLA-F and HLA-F-AS1. The "AS" part means, "anti-sense", so it's on the opposite strand...so ignore all of the HLA-F-AS1s.
Note the associated chromosomes. chr6 is a normal chromosome, but things like chr6_cox_hap2 aren't. Instead, these are haplotype patches/chromosomes. The HLA regions are highly variable, so having only a single reference sequence ends up being problematic in many analyses, such as finding sequence variants. For your purposes you may or may not want to ignore these, it depends on what your goal is.
If you ignore the haplotype patches then you're left with 3 listings on chr6. These are the 3 isoforms of HLA-F. You end up needing to use the refseq IDs for each of these.

BTW, Gencode/Ensembl list 4 isoforms for HLA-F, rather than 3. Whenever UCSC disagrees with Gencode or Ensembl, go with Gencode or Ensembl.

Many thanks for your nice reply. Just one thing, would you please help me out how to get Refseq sequences of interest from Ensemble in a way that the CDS is recognizable from UTRs in the sequences?

Google "Biomart".

Would you mind justifying your last statement? >Whenever UCSC disagrees with Gencode or Ensembl, go with Gencode or Ensembl. Not that I disagree, but it would be better to give a reason for suggesting some source is better than another.

UCSC's annotations have historically been a bit of a mess. For example, they have genes with the same ID on multiple chromosomes and strands, which will break a number of tools. refSeq in particular tends to be overly conservative in what it includes, so typically using it results in missing a number of likely correct isoforms. For what it's worth, UCSC now defaults to Gencode for human (and Gencode is essentially the same as Ensemble)

@DevonRyan Thanks. Maybe this paper is also relevant.


text:
What is the convention for indicating genomic primer sites?
What is the most common notation for indicating genomic binding sites of primers relative to an ORF?
For instance, if I want to indicate a primer like so:
...tccgccGCCCGTCCACACCCGCCGCCagctcaccATGGATGATGATATCGCCGCGCTCGT...
         [ Primer           ]        [ Hs ACTB coding sequence   ]

Should the location of this primer be indicated as -8 or -28 (from ACTB start codon) or something else?

Personally, I would say something about the forward primer spanning nucleotides -28 to -8 from the ATG codon, and perhaps give a reference to the nucleotide positions in either the genomic sequence NC_000007.14 (ACTB is on the reverse strand) or the mRNA sequence NM_001101.3.

There is no such convention. People, mostly name their primers arbitrarily (or just FP and RP) and mention in the text about their binding sites.
In general, in the context of specific genes, the positions are described with respect to the transcription start site (TSS).


text:
Why the length of UTR in the genomic sequence of gene X is too much longer than the same region in the corresponding Refseq mRNA sequences?
I'm browsing in the UCSC genome browser and found that the UTRs length of KIAA0040
gene in the genomic sequences is too much longer than the corresponding the Refseq mRNA sequence. In fact, the total length of Refseq mRNA sequence is 4,721 and the length of its genomic sequence is about 36,107bp, of which the length of CDS is just 300 bp. How to explain this event?
This gene has 4 transcript variant and I know something about that UTR can span multiple exons, but I'm not sure about it and would like to hear more from you.

Doesn't the genomic sequence you refer to contain intron sequence?

What do you mean by "length of the gene" ? The UCSC browser displays the mRNA sequences aligned to the genome, so the sequences can differ only if there were errors in alignment. Are you saying the UTR is longer in the genomic alignment than in the refseq mRNA sequence? Which mRNA are you referring to?

UTRs are involved in post-transcriptional regulation. See the wikipedia articles on the 5' and 3' UTRs. Alternative splicing of UTRs allows for exposing/hiding these regulation sites, which may then be useful for differential regulation in differing tissues.


text:
Which primates can swim underwater?
I saw a documentary awhile back and they were profiling a certain species of monkey which regularly swims underwater. I can't recall which species it was but they said it was rare for primates to do this - diving under the surface, holding ones breath, and swimming completely submerged.
I'm wondering which type of monkey this was and what other primates, besides humans, are known to engage in underwater swimming? Is there a reason this behavior evolved? My guess is that it has to do with foraging for food in mangrove type environments and possibly for avoidance of predators.

The Allen's swamp monkey (Allenopithecus nigroviridis) is also know to live near water-rich areas and they sometimes dive to avoid danger.
Also, it was recently shown that the chimpanzee (Pan troglodytes) and the orangutan (Pongo) can swim, dive and even retrieve items form the bottom of a swimming pool. (source)

The proboscis monkey (Nasalis larvatus) is a species of monkey which remains underwater. They usually found near large water bodies. And can swim up to 20m (66ft).


text:
How does this headless fish still move?
There is a (VIDEO) on Facebook where the fish starts to flail around despite no heart or internal organs.
What causes the fish to flail around the way it does?
My theories:

It is because of pressure causing the muscles to contract - much like when you leave your own hand loose and squeeze up your arm making your fingers curl.
It is because the nerves are still alive - much like how you can rub the fish heart the right way and cause it to beat again even though the fish is very much dead. (I watched my fifth-grade teacher do this in class)

I had actually heard a research talk related to this. It happens because of spinal reflex.

It is a widely known spinal reflex arc which causes decapitated animals (even soldier without head) to move over some period of time after decapitation.
One of the arc representations:

see also The life after decapitation
additional video


text:
What kind of beetle is this (2cm long, brown, "V-shaped" body)?
I've seen this brown beetle, which was about 2cm-3cm long (I guess) near Loch Lomond (Scottland) a few days ago.

What kind of beetle is it?

Now it's free to use: https://commons.wikimedia.org/wiki/File:Stink-bug.jpg

I agree, it is a forest bug. But be careful, when someone kills it, it produces a extremelly bad smell.

Honestly, that looks like a stink bug, family Pentatomidae.
You can see some slightly different coloured ones here on Insects of Scotland
Here is a photo of the one that I used to see in the States (From Master Gardening):

More commonly referred to as shield bugs in the UK.

It's not a beetle but a shield bug, probably a forest bug (Pentatoma rufipes): Wikipedia. The Collins Complete Guide to British Wildlife describes these as widespread in the UK, with adults seen from August to October.
Beetles are from the order Coleoptera, bugs ("true bugs", rather than the informal use of the term to mean, basically, any creepy-crawly) are Hemiptera. Beetles have two pairs of wings, but the front pair is hardened and acts like a shell and only the rear pair is used for flying. Bugs have either one or two pairs of wings. The front half of the forewings is usually hardened for protection, but the rear half is unhardened; if there's a second pair of wings, they're usually unhardened and all wings are used for flying.

In some insects one of the pairs of wings is modified into halteres.

Pentatoma rufipes would be my suggestion as well, without knowing the Pentatomidae fauna of the british islands in particular.

@fileunderwater Good point. I added a reference attesting to them being common in the UK.


text:
Why do the deoxyribonucleotides use T and ribonucleotides use U?
We all know deoxyribonucleotides form DNA while ribonucleotides form RNA, DNA is double stranded while RNA is single stranded, and RNA can transcribe from DNA. We also know that DNA use A, G, C, T, while RNA use A, G, C, U and that it's the DNA that stores genetics information, not RNA.
My question is: how does the lost oxygen atom on deoxyribonucleotides 2' site of the sugar (turning it into a ribonucleotide), make such a large difference in function? It just an oxygen atom. Why don't they just all use U or all use T?

Why deoxyribose for DNA and ribose for RNA?
This answer may solve the question why is DNA double strand, RNA single strand, but it doesnt explain why does RNA uses U instead of T.

The question isn't really the same, but the (excellent) answer to the linked question probably answers this one.

RNA can and does form double helices, either through intrastrand base pairs or between strands. http://biology.stackexchange.com/questions/19115/what-makes-dna-helical/19119#19119

"My question is, all the different is due to the deoxyribonucleotides lose an oxygen atom on the 2' site of the sugar, how could be so much different? It just an oxygen atom." Hydroxyl groups are more reactive than a hydride group. The 2' -OH can be deprotonated and react with the Phosphate in the backbone of the RNA molecule and break the phosphodiester bond and cyclize with the phosphate attached to the 3' carbon. The 2' -H cannot react with the phosphate group, so the phosphate backbone of DNA is more stable than an equivalent RNA molecule in that regard

The difference between the T and the U likely has more to do with the enzyme catalyzing the synthesis reaction https://en.wikipedia.org/wiki/Nucleotide#Synthesis and is not directly related to the 2' - hydroxyl.

"It just an oxygen atom". Umm... If you remove an oxygen atom from water, you get a highly flammable gas and not something you would drink to quench your thirst. There's no such thing as "it's just a single atom". Changing an atom is a huge difference.

For the switch from thymine (T) to uracil (U), it actually doesn't have anything to do with the sugar backbone of the nucleotides. This article on Science Daily explains that U is more cost efficient to produce than T because it can be easily gotten from a chemical degradation of cytosine (C). Since RNA has a short life span and because the cell needs a lot of RNA it uses U. DNA, on the other hand, undergoes a lot of checks and repairs. If it were to use U, it wouldn't know if the U was really a U or if it was a C that got damaged. Since it is important to keep the number of mutations to a minimum, DNA uses the more costly T to ensure fidelity.
I would also like to point out @AMR's comment. It isn't just an oxygen atom. An oxygen atom is the difference between the air we breath and ozone that can kill you. It's the difference between water and highly flammable hydrogen gas.

RNA forms double stranded structures!

dsRNA is thermodynamically more stable than dsDNA, actually.

@canadianer The A, B, and Z forms of ds helicies is an artifact of in vitro preparation of the molecule related to the the salt content and consistency of the humidity during the crystallization process. This does not mean that we actually see these structures in vivo, though for DNA, our best model if B. And as I asked on a different thread, is the thermodynamic stability related to the hybridization and thus melt temps needed to open dsRNA or is the relationship actually referring to the stability of the molecules sugar-phosphate backbone.

2'-OH can and does get deprotonated and can then attack the phosphate,  breaking its bond with the 5' carbon of the next nucleotide it the chain. The phosphate and 2'-OH cyclize and the backbone is broken and broken chromosomes lead to apoptosis and cell death, so using an RNA double helix for chromatin would be riskier. Also, it may not be an advantage in larger genomes to have a molecule that is thermodynamically more stable, as this would likely slow and/or increase the energy required to replicate that genome.

@AMR There is a difference in Tm. See, for example, this paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC331958/pdf/nar00044-0318.pdf

@canadianer Thank you for the link. It might be a bit difficult to draw genome wide conclusions from 24bp strands, but I am sure that the results are accurate. Adding to my comment above, I also wonder how ribonucleotides interact with histones or if they can, as packing becomes a very important and highly conserved chromosomal element as genome size increases.

@AMR The only conclusion I'm drawing is that dsRNA is thermodynamically more stable than dsDNA.

@canadianer Your observation is correct, and in retrospect I think that the meaning of the last sentence of the answer is unnecessarily vague. Your point regards hybridization stability and I can see where SolarLinux comparison may not be valid from that perspective, however, RNA molecules degrade more rapidly in the sense that their backbones are prone to breakage because of the mechanism I mentioned before. In that respect, DNA is a more stable molecule as it will not break in this manner, making it more suitable for information storage than dsRNA.


text:
Overcoming Inbreeding Depression
When inbreeding depression occurs, a genetically unrelated individual is mated with the animal to introduce genetic variability and remove homozygosity. In this case either outbreeding or crossbreeding may be carried out. Is there any preference for either technique over the other?
Out-breeding here refers to mating between two individuals in the same breed, but no recent common ancestors.
Cross-breeding refers to mating between two individuals of different breeds entirely.

can you clarify language? Is it that outcrossing is mating between different populations, whereas crossbreeding is mating between members of inbred populations? E.g. mating between european and asian peasants versus mating between members of european and asian royal families.

this article mentions both outcrossing and crossbreeding. Language seems confusing to me

I don't think there is any accepted clear definitions of outbreeding vs crossbreeding. Therefore, definitions should be provided in the post.

@Remi.b my point exactly. Although, broadly, if you cross inbre(a)d species, you get less variation than crossing more wild-typish (forgive me) animals


text:
Dragonfly Identification
I have been clearing brush by a lake in northwest Missouri and seen a lot of dragonflies. It's hard to get decent pictures because my phone camera sucks and they fly away before I get close. But here is one I managed to get:

I got one other picture of another species, but it's much lower quality.

The first one is a blue dasher (Pachydiplax longipennis).
Sorry, I couldn't identify the second one but it is more probably the same.

Did you want to edit this further? I was reluctant to accept it right away, but I think you're correct on the first one. The second one is probably too blurry to tell much.

@user137: Thanks. I completely forgot about this one. I still think they both are the same. source:  http://www.insectidentification.org/insect-description.asp?identification=Blue-Dasher

The overall body shape of the second dragonfly looks like a Libellula (Skimmer), due to its broad flat abdomen. It also seems to have distinct bands on all four wings, dark patches where the wings connect and a light blue abdomen, which would indicate e.g. a male Plathemis/Libellula lydia (Common whitetail). The picture is blurry though, and there might be other similar species that it can be mistaken for (the wiki page mentions a couple of similar species).

(picture from wikipedia)

It looks right to me. I probably should have split this into 2 questions so I could have two answers.

@user137 Well, its difficult to know in advance whether you've seen one or two species.


text:
Why are siblings unidentical? (Which chromosome of the pair do gametes have?)
I know that a normal human cell has 23 pairs of chromosomes (total: 46).
On the other hand, a gamete has only 23 chromosomes.
Which chromosome does the gamete choose out of each pair?
And if "One of each pair of chromosomes comes from the mother, the other from the father.", then the chromosomes of a gamete could be an exact copy of the chromosomes in a grandfather's gamete?

Have you read the basic Mendelian genetics; check the law of independent assortment.

Therefore, there are many levels of variation.

The gamete doesn't "choose" one or the other.  Both are made and you get two gametes, one for each.
Also it's unlikely to be an "exact copy" due to recombination and random or independent assortment.  There are also smaller influences on genetic variation, and epigenetics, but at this level of question I think you should focus on those two.
Was this homework?  If so it should be tagged.

Also there is random assortment, so even without taking recombination into account there are 2^23 possible combinations for assortment, or about 8.5 million combinations. Throw recombination into the mix and you start to see why there is so much variety, even among siblings.

No this is not homework, just personal study, but thanks for your answer, it was well worth a read.

Great links as well!


text:
What is a holocentric chromosome?
I was doing this question that asked: "How many centromeres does a typical chromosome have?"
I thought one and the answer was:"One, except for holocentric chromosomes."
So then what are "holocentric chromosomes"?
I assume they would be chromosomes with more than one centromere, but then why do they need more than one centromere? And where can I get some more information on them? I tried googling but did not find much info on this.

I believe that you did the search but are you sure you spelled it correctly? Autocorrect may have changed it to Heliocentric Also are you using Google in a country other than the US? When I Google holocentric chromosome, the first two entries were NIH (National Institute of Health) Articles, then Images of Holocentric Chromosome, then the third was the English language Wikipedia article on Centromeres. It is possible that Google in another country will not have the same results as these.

I got the same results as you did. I didn't click open the NIH article, which proved to be quite helpful.

No worries. I was interested in seeing if maybe you were outside of the US and that would have been why you might not have gotten the necessary results. Thanks for responding!

In most eukaryotes, the kinetochore protein complex assembles at a single locus termed the centromere to attach chromosomes to spindle microtubules. Holocentric chromosomes have the unusual property of attaching to spindle microtubules along their entire length.

source


text:
Dwell time equations for ATP-sythase?
I have read that every 120 degree rotation of the F1 complex of ATP-synthase can be split into a 30 degree rotation and a 90 degree rotation. In between these two are dwell times, the one before the 90 degree rotation been called the ATP-binding dwell time and the one after been called the interim dwell time and that both of these fall of exponentially. I cannot, however, find a derivation of the probability density function of these dwell times, or there exact form. If anyone knows such a derivation or where to find one this would be much appreciated.

Are you asking for the mathematical model or the experimental measurements ?

@WYSIWYG The mathematical model

Usually, the dwell time between independent reactions is exponentially distributed. You can have a look at this paper for a biophysics based mathematical model.

@WYSIWYG I am pretty sure that one depends on the concentration of atp present though

The rate of binding depends on the concentration of ADP (the substrate) but not the rate of conversion to ATP.

@WYSIWYG sorry I was thinking of ATP-hydrolysis (which I think the F1 complex can do). I think the relationship is along the lines of $p\propto ce^{-kct}$ for the binding site dwell time (where $c$ is the concentration of AD(T)P), but I have no idea how to derive it.

That is based on a simple first order kinetics... The dwell time distribution can be derived from the probabilistic  "master equation" for the reaction.. Your distributions of reaction probabilities can be modelled by Poisson distribution and conversely the dwell times would follow exponential distribution..

ATP Binding dwell time
Here is a very dodgy derivation of the binding dwell time (note I am the OP). For this we have $$E+S\rightarrow ES$$
Where $E$ is the enzyme and $S$ is the substrate (keeping this general). We can write our rate equation as:
$$rate=k[E][S]$$
But we can also write the rate as:
$$rate=-\frac{d[E]}{dt}$$
so that:
$$\frac{d[E]}{dt}=-k[E][S]$$
Now here is the bit that I think is a bit dodgy, we are going to assume that $[S]$ is approximately constant. So that:
$$[E]=Ae^{-k[S]t}$$
We can take $n=[E]V$ to represent the number of enzymes left, where $V$ is the volume, then letting $n_0=VA=constant$:
$$n=n_0e^{-k[S]t}$$
The probability of been within the time $t$ is then given by:
$$F(t)=1-e^{-k[S]t}$$
Which is our commutative distribution function. Differentiating this gives our probability density function:
$$f(t)=k[S]e^{-k[s]t}$$
Interim dwell time
The interim dwell time (also called the catalytic dwell time) involves two steps[7]:
1. The cleavage of the enzyme bound ATP.
2. The release of the hydrolysed products.
Each of which is going to follow the distribution (analogous to the above) of:
$$p_i(t)=k_i e^{-k_i t_i}$$
For $i=1,2$ respectively. The joint probability distribution is found by the convolution of these two [8]:
$$p_T(t)=\int^{\tau}_0 p_1(t) p_2(\tau-t)dt$$
Which gives:
$$p_T(t)=\frac{k_1 k_2}{k_1-k_2} (e^{-k_2 \tau}-e^{-k_1\tau})$$
Edit
Although starting from deterministic equations (which actually doesn't really matter), this method does hold and is simple. The type of reaction is called a pseudo-1st-order reaction (or 2nd order class 2) which explains my approximation for $[S]$ been constant. See [9] and [10]
Sources for additional info

https://youtu.be/X_YXTWU2maY?list=PLbKSbFnKYVY3j6ubaW1zgTXj5C4443v8s
http://www.nature.com/articles/srep08773
http://www.ks.uiuc.edu/Research/atp_hydrolysis/
http://www.pnas.org/content/85/17/6314.full.pdf
https://books.google.co.uk/books?id=uIxwICNmLKEC&pg=PA199&lpg=PA199&dq=catalytic+dwell+time+distribution+%5Batp%5D&source=bl&ots=u8oBcVNCDc&sig=PKvdVAwT0WxdqTuVwMxhU3RfSwM&hl=en&sa=X&ved=0CCAQ6AEwADgKahUKEwiGhKDalufHAhXkadsKHc54ADs#v=onepage&q=catalytic%20dwell%20time%20distribution%20%5Batp%5D&f=false
http://crystal.harvard.edu/PDFs/floyd_biophysj.2010.pdf
http://www.ncbi.nlm.nih.gov/pubmed/16258036
http://crystal.harvard.edu/PDFs/floyd_biophysj.2010.pdf
http://glutxi.umassmed.edu/grad/GradKinetics.pdf
http://chemwiki.ucdavis.edu/Physical_Chemistry/Kinetics/Reaction_Rates/Second-Order_Reactions/Pseudo-1st-order_reactions

You cannot obtain probability distributions from these deterministic equations.

@WYSIWYG Please can you explain, the equation $n=n_0 e^{-k[s]t}$ is equivalent to that for nuclear decay, which gives an equivalent probability density to that I have given.

It will not give you probability distribution because this rate is based on deterministic mass action kinetics.. You have to represent your equations in terms of probability instead of reaction rates to obtain those equations... Have a look at chemical master equations

@WYSIWYG I asked (and then when I came up with an answer, answered) the following question on Chemistry.SE I think my answers  provides a replacement for the first part of the derivation using the master equation: http://chemistry.stackexchange.com/questions/37074/master-equation-for-catylist-and-substrate-binding

check my answer on Chemistry.


text:
Why does a coconut have exactly three "holes"?
Why do coconuts have exactly three "holes", as seen in this picture?

A theory says:
As coconut is a sibling of palm, somehow long time ago, three palms were in a same husk. Based on evolution theory, it's how the coconut was born in the world with three holes.
Reference:
"Why does a coconut have exactly three eyes?", Quora

I'm not exactly sure what your question is. Are you wanting someone to clarify or confirm this theory?

That's not evolutionary theory, that's mythology.

Is this a question?  If so, it desperately needs an edit.

Based on strictly on evolutionary theory: "because it can".

This was necessary to invent bowling.

The three "holes" are the result of the 3 carpels in coconut flowers, and three carpels is typical of the family Arecaceae (Palms). The "holes" are actually germination pores, where one is usually functional and the other two are plugged. The new coconunt shoot will emerge from the functional, open, germination pore.
For further info and pictures, see this webpage or the paper Morphological and anatomical studies of the coconut (Smit 1970, link to pdf), which holds a wealth of information.

This must be truly the answer with the highest vote-to-text ratio ever! +1


text:
How C. Elegans is used for siliencing genes
The experiment that is using C. Elegans to silence the Genes. I have a question about Why and how C. Elegans can use the DNA plasmid that is generated with the gene of interest in the bacteria by being fed the bacteria?

If you describe your procedure in a little more detail it will be easier to tell exactly what you are doing, but basically the cells of the C. Elegans can be induced to take up the plasmid and that can be transcribed by an RNA polymerase. The Messenger RNA is then translated by the ribosomes to produce a protein that inhibits the transcription of the gene of interest. If it is RNAi, then the RNA produced will hybridize with the mRNA transcripts that are being produced by the gene of interest. dsRNA cannot be translated and even if some of the mRNA is, the protein will be nonfunctional.

If you are actually doing recombination, then you likely linearized your plasmid with a restriction enzyme and the plasmid has homology arms that will allow it to be combined into the genome of the worm's cells. The success rate is usually low without some form of technology like CRISPR or Talens, so if you are using those, then there is likely some form of targeted DNA break that is happening to allow for homologous recombination to integrate the linearized plasmid into the chromosome of the worm.

It sounds like you are performing RNAi... this procedure explains what is going on. http://www.jove.com/science-education/5105/rnai-in-c-elegans They take the bacteria up in vesicles, digest then which releases the RNAi that the bacteria has produced and that intern goes on to hybridize with the mRNA of the gene of interest, as I said above, that binding either stops translation altogether or the protein product is no functional.

If it's what I'm thinking of, you probably have GFP+ worms that end up getting fed some DH5-α E. coli that were transformed using CaCl2. The outcome is your control worms should nicely fluoresce, and the experimental worms will be a noticeably weaker color. The RNAi process is explained nicely in that link provided by AMR.

Thank you AMR and Kendall for explaining this to me!! and Thanks for the video. It helps a lot to understand the concept. Thank you!!!

From the way that you have described your experiment, feeding C.elegans bacteria that are expressing a plasmid that will induce gene silencing, then both @Kendall and I think that you are likely performing an RNAi (interference) experiment.
As @Kendall writes:

If it's what I'm thinking of, you probably have GFP+ worms that end up getting fed some
DH5-α E. coli that were transformed using CaCl2. The outcome is your control worms should nicely fluoresce, and the experimental worms will be a noticeably weaker color. The RNAi process is explained nicely in that link provided by AMR. –  Kendall

The bacteria will transcribe RNA molecules encoded by the DNA plasmid. These RNAs will have complimentary sequences to sequences from your gene of interest.
When the nematode eats the bacteria, they RNA molecules that the bacteria has produced will be taken up by the cells of the worm.
The Dicer enzyme then cleaves the dsRNA into small fragments. These fragments are then able to hybridize with the mRNAs transcribed from the gene of interest. This will either cause the ribosomes not to bind properly or will start translation out of frame or without key amino acids or will terminate translation early.
The net effect is that the cells will either not produce the protein encoded by the gene of interest or will produce a non-functional protein. If, as @Kendall said, the gene of interest is a reporter gene such as GFP, then the result of the interference experiment will be C.elegans that do not fluoresce. If the gene of interest is a structural protein such as actin, then you will see the effects of knocking out the actin gene on the cells of the worm.
This online video protocol from JoVE.com gives a detailed overview of the RNAi in C.elegans experiment and also demonstrates how the protocol is carried out.


text:
IBD-value in pedigree with inbreeding
I have a question about IBD. Please see the figure below. How many pairs of alleles are IBD for X and Y, or what is the IBD value for X and Y. Is it four (4)? I have seen it to be maximally 2, but then we assume that no inbreeding occurs, right?

An Identical-By-Descent (IBD) value is the number of alleles which are the same because of descent from a common ancestor.  Since each (diploid) individual has two alleles for a given (autosomal) gene, the number of them that are IBD with another individual can only be 0, 1, or 2.
In your example, X and Y inherit each of their alleles from A2, so their IBD value is 2.  Inbreeding is just an extreme form of descent from a common ancestor; it causes on average greater probability of high IBD values than when comparing less-inbred individuals. See the passage here for more detail.

Thanks for answer @mgkrebbs. I am still a little bit confused. This is due to the following excerpt from Thompson: Pedigree Analysis in Human Genetics, 1986, The Johns Hopkins University Press, page 28: "Consider now a pair of relatives, neither of whom are inbred, although their parents may be. Since neither of the two individuals can carry two identical genes, there are only three possibilities of gene identity (figure 11): the individuals have two genes in common, or one or neither." Does the IBD value relate to only one person or to the two individuals under consideration.

Hmm. I see three possible solutions: 1) the individuals share 1 allele IBD, the a allele 2) the individuals share both of their alleles IBD so that IBD=2 3) all the alles are IBD, so that IBD=4 (you can make 4 different pairs of IBD alleles). It looks Thompson and the excerpt you provide look at the two persons at the same time; i.e how many alleles do two persons share . It looks like they do not look on the individual level (i.e how many of the alleles of.one person does the individual share with the other.)

If we assume that @mgkrebbs' solution is correct, what would the IBD-value be between R and X if R had genotype ca instead of cd? Now R has one allele in common with X, but X has two alleles in common with R.

IBD (and IBS) is a characteristic of the relationship of two persons' genes, not a characteristic of a gene or allele itself.  So the only possible relationships  are: no alleles are the same, one pair of alleles are the same and one different, or both pairs of alleles are the same.
If R' is ca, then R' and X have IBD (and IBS) value of 1 -- they have one  pair the same.  The alleles are unordered - you choose the pairings between individuals' alleles so as to maximize the IBD count, having chosen one pair, the other pair is also determined, being the only pairing that can then exist.


text:
Cell-type specific methylation profiles: original reference finding?
This is a general question, and a specific question. I'm looking for the original reference that first talked about how DNA methylation profiles are cell-type specific.  This is specific, because I care about this specific reference paper, but it is general because I don't know how to go about finding original reference papers to begin with.
Any help would be super appreciated!

Note: This is not my field, and only the result from a quick  database search

Doing a quick search in the Web of Knowledge, I found the paper Ehrlich et al (1982), Amount and distribution of 5-methylcytosine in human DNA from different types of tissues of cells, which is relatively well-cited. This in turn mentions that:

Recent studies indicate that for many genes associated with vertebrate development, there are tissue- or cell-specific differences in the extent of DNA methylation.

The oldest studies referenced in this paper that seem to refer to tissue-specific methylation are Vanyushin et al (1970), Rare Bases in Animal DNA, Nature and Vanyushin et al (1973), The content of 5-methylcytosine in animal DNA: The species and tissue specificity, Biochimica et Biophysica Acta. The 1973 paper is also one of the earliest papers cited in another well-cited paper from 1983 (Gama-Sosa et al, 1983)), so it might be the best bet. However, Gama-Sosa et al also mentions Kappler (1971), The 5-methylcytosine content of DNA: Tissue specificity, which is clearly relevant. In total, Gama-Sosa et al has references to 13 early papers on DNa methylation, so you might want to check them all out, and backtrack from there. Also, Vanyushin seems to have published in smaller, more obscure journals around the same time (e.g. DOKLADY AKADEMII NAUK SSSR), so there might be earlier papers that express the same ideas. The earlier papers seems to deal with bacterial DNA methylation though.
A couple of other references are:

Van der Ploeg & Flavell (1980), DNA methylation in the human gamma delta beta-globin locus in erythroid and nonerythroid tissues,
Mandel & Chambon (1981) DNA methylation: organ specific variations in the methylation pattern within and around ovalbumin and other chicken genes
McGhee & Ginder (1981), Specific DNA methylation sites in the vicinity of the chicken beta-globin genes


text:
It's right to say coding sequence is part of exon sequence?
Some basic ambiguities making me confused. I downloaded 5'UTR, CDS, 3'UTR, and exon sequences, separately from Biomart for a gene P4HA2 (Homo sapiens) and found some simple sequence repeat (SSR) on them. While there is a repeat x on the exon sequence, it was not located on the 5'UTR, 3'UTR, and coding sequence (or CDS) of gene. As I remember, exon sequences is the same with coding sequence, except for the first and last exon, which are parts of 5'UTR and 3'UTR, respectively, am I right?. Could you please help me out to find how the mentioned event is possible?
Thanks

Are your comparing the same splice variant?

As @canadianer said, remember that almost all human genes are interrupted. There are long intronic sequences in the gene that can interrupt your coding sequence. Also alternative splicing can cut out exons that make up the mature mRNA. If you do an alignment you should be able to pick up where the exons are in the splice variant of your gene.

Yes Canadianer, I compare the same splice variant.

As I remember, exon sequences is the same with coding sequence, except
  for the first and last exon, which are parts of 5'UTR and 3'UTR,
  respectively, am I right?

Not necessarily. The UTRs can be composed of multiple exons and there can be an exon that spans both sides of the start codon i.e it is both a part of the 5'UTR and CDS. Similarly, an exon can span both sides of the stop codon.
A reason for why you are not able to map your repeat to any of the regions of the mRNA could be that your repeat falls in an exon that spans the start/stop codon. The repeat itself might span these sites. You need to provide additional details such as the location of the repeat, size of the repeat and which exon it maps to. Also mention which reference genome file are you using.

The coding region is that region of the DNA coding strand that is translated into a product. This is synonomous with the exon region. The 5' untranslated region and the 3'untranslated region are just that and though they may serve some little understood function in replication, they are not translated into a protein. "coding region" is not a term that I have heard widely used although I am a neophyte as a molecular biologist.


text:
Will bacterial promoter without either -10 or -35 sequence allow no transcription?
I have a strong constitutive promoter on a plasmid inside of E.Coli, which expresses a gene. Having either -10 or -35 sequence modified to random sequence, will it ensure zero transcription from that promoter?
Thanks.


text:
Consumption of different type of energy when one is inactive
I'm wonder if there is any study done on this and what are the results?
how much of each type of energy one's body(healthy normal person) uses when inactive(seating down)
I know there are alot of dependencies, but any kind of ball park answer will be great.
ps: when I say type of energy, I mean: fat, carb, protein.

Simple google search gave this ! Good enough to answer your question.

Thank you for this link, but it doesn't provide me with any precise numbers I'm looking for.


text:
How to interpret this cuffcompare result? Sensitivity over 100?
I run a cuffcompare:
cuffcompare -r transcripts.gtf TransStandard_1.0.gtf

I got the following result:
#= Summary for dataset: /home/tedwon/Sources/QA/data/trans/TransStandard_1.0.gtf :
#     Query mRNAs :     165 in      78 loci  (157 multi-exon transcripts)
#            (69 multi-transcript loci, ~2.1 transcripts per locus)
# Reference mRNAs :     165 in      78 loci  (157 multi-exon)
# Super-loci w/ reference transcripts:       77
#--------------------|   Sn   |  Sp   |  fSn |  fSp
    Base level:     100.0   100.0     -       -
    Exon level:     110.6   110.6   100.0   100.0
  Intron level:      99.6    99.6    99.6    99.6
Intron chain level:     100.0   100.0   100.0   100.0
  Transcript level:     100.0   100.0    99.4    99.4
       Locus level:     100.0   100.0   100.0   100.0

 Matching intron chains:     157
          Matching loci:      78

      Missed exons:       0/872 (  0.0%)
       Novel exons:       0/872 (  0.0%)
    Missed introns:       3/756 (  0.4%)
     Novel introns:       0/756 (  0.0%)
       Missed loci:       0/78  (  0.0%)
        Novel loci:       0/78  (  0.0%)

 Total union super-loci across all input datasets: 78

What I don't understand is that why the sensitivity and specificity for the exon level are over 100? The values in this example are both 110.6. Shouldn't it be from 0% to 100%? The website doesn't address it.

Can you please format the output properly (adjust the tabs so that the lines are aligned)

I don't know if this is still needed but I went through the source code of cuffcompare to see if this phenomenon is indicative of the false positive rate or an issue with the tool (and to provide a more thorough answer). It seems like it may be a bug in the code for cuffcompare (which is a massive amount of code). If you look at line ~1518 in the source code at this URL:
https://github.com/cole-trapnell-lab/cufflinks/blob/master/src/cuffcompare.cpp

There are several statements that suggest Sn values > 100% would be possible and should be reassigned to 100%. These results may occur from keeping "redundant" transcripts if they start with the same 5' intron. How do your "fuzzy" Sn and Sp compare to this result? are they are similar?
The developers are no longer maintaining this software in favor their new faster version, Hisat/Stringtie. However I find the output to be more complete from Tophat and Cufflinks. To get a better understanding of the output, you could compare the number of potentially novel features in your cuffcmp.combined.gtf to the total number of features in your new cuffcmp.combined.gtf using overlapping and contained features as a proxy for false positive rate. Comparing these values with the total number of lines in your reference annotation may provide you with another Sn estimate without performing qPCR.
# to count the number of potentially novel
grep -c "\"j\"" cuffcmp.combined.gtf

# to count the overlapping and contained features
grep -c "\"[c,o]\"" cuffcmp.combined.gtf

# to count the number of exact matches
grep -c "\"=\"" cuffcmp.combined.gtf

# To count how many features are identified for each gene
cut -f4  -d ";" cuffcmp.combined.gtf |   uniq -c

# To count how many known genes gene were identified
cut -f4  -d ";" cuffcmp.combined.gtf |   uniq -c | wc -l

# To count number of features in the reference gtf
wc -l reference_annotation.gtf

or if you prefer to use Bioconductor packages like rtracklayer in an R environment, you could read the cuffcmp.combined.gtf file and analyze the data further
library(rtracklayer) # if you have the package installed
rtracklayer::readGFF("~/full/path/to/cuffcmp.combined.gtf")

is that science direct an open access article? if not, some users may not have access. Also, you may want to check out the how to best answer a question in the help center http://biology.stackexchange.com/help/how-to-answer it would definitely improve your answer if you added some background and links to other users to follow along - thanks for your efforts!

@Drew The Evaluation of Gene Structure Prediction Programs paper does give the definitions but nowhere it define how sensitivity can be over 100%.

@Drew I believe this is a bug as sensitivity over 100% is totally unacceptable. This is like probability over 1.

I thought that this might be the result of including novel features in the cuffcmp.stats output which are added to the numerator but not to the denominator of the Sn and Sp calculations.  However, given that your output lacks novel features and produces greater than 1 Sn and Sp calculations, that assumption is incorrect.   It  may be a small enough task to modify the source code on your local workstation.

https://github.com/cole-trapnell-lab/cufflinks/blob/master/src/cuffcompare.cpp

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
difference in genetic instuctions between male and female
I'm a computer science graduate so please bear with me the following computer program :
mov  ecx, -1
INC  ecx
consist of 2 instructions (mov,inc) each working on specific data , can genetics instuctions be expressed in the same way ? if so what is the difference between male and female(humans) when it comes to the number of instructions and the difference if any (eg , n-instuctions being exclusive to female ... etc) ?
Edit#1
:what I mean by instructions is something like a computer program and a programming language commands.

I don't know what do you mean by Instructions ? Can you be more clear ?

As many biologists, I don't know assembly. If possible, can you rewrite your 2 instructions into C, python, R or some other commonly used languages?

As argued here, the analogy between genetics and the digital world can be quite misleading and one should make sure to not push it too far. I think there are 2 questions in your post: "Is there an equivalent to ?" and "Do human male and female differ in their number of 'instructions'?". You should always try to restrict your posts to one question only.

The typical Male has a Y-chromosome, which consists of about 100 genes.
Genes are the instruction sets to make proteins, and proteins do the work of the cell.
Those 100 genes out of about 21,000 in the human genome are what differentiate Males from Females.
That being said, because of how signaling works, Males and Females can exhibit different expression patterns, like function calls, even though they have the same instruction sets, for the most part.
Expression patterns are how genes are activated and deactivated, it is basically a regulatory process that controls the functions of the cell, tissues, organs, and organism.

There are many other things besides the 100 genes on the Y chromosome that differentiate males from females. If that was the case, XXY persons would be clearly male, when they are not. X genes play a significant role, as do somatic genes.

@MattDMo that is why I chose my words carefully. I said the "typical" male and mentioned that expression patterns can differ. Based on the basic nature of the question I didn't think that it was necessary to go into the intricacies of cell signaling and signal concentration as it relates to gene expression, however if you feel it is necessary to expand the answer to include that level then please feel free to expand on it.

@MattDMo A person with Klinefelter's syndrome (XXY), assuming that they do not also have an SRY reversal are considered to be males genetically. The phenotype comes from the additional dose of expression from the Barr bodies, as they are not completely silenced. XXY in drosophila is genetically female, but for humans, they are sterile males. This Bio SE answer http://biology.stackexchange.com/a/3317/16651 provides a chart that corresponds to the 5th Edition of Genetics by Hartwell et.al.


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How quickly can lasers of various wavelengths and powers impair human vision or cause pain in the eyes?
There is a discussion on HackerNews about how self-driving cars might be susceptible to confusion attacks using a cheap laser pointer and a RaspberryPi.
Some people argue that human drivers, too, are susceptible to attacks by laser pointers.
For lasers in the visible spectrum, I'm pretty sure that the human driver can tell he/she is under attack very quickly. But how about lasers outside the visible spectrum? Since you can't see the laser, the only way you can tell something is wrong is if your vision is impaired or you feel pain in your eyes. How quickly can that happen?