Field of Science

In Support of Unions: Atheist Talk this Sunday

Monica Meyer
Monica Meyer will be joining Mike Haubrich to discuss the campaign against unions in this country. Yes, they will be discussing gay marriage on Atheist Talk Sunday March 27th 9AM Central on AM 950.

Our guest this week will be Monica Meyer, executive director of OutFront Minnesota.  She will discuss their upcoming Lobby Day at the State Capitol in St. Paul on April 14, 2011.  She will also discuss the threat of the Minnesota State Legislature putting a State Constitutional Amendment on the ballot that would specifically ban same-sex marriage.

You can live stream the show, simply enter a Minnesota zip code, like 55455.

Does size matter...or shape..Yes we're talking about the penis

An older
study brought to my attention recently (subscription required, though I also found this link).

This is strictly to avoid a dong
being the lead in picture on FoS

The authors want to test some ideas regarding behaviors and adaptations human males may have to ensure paternity. As I heard about this research, my skeptic meter went off and I whipped out my critical thinking tool box to look at this problem and research more closely. The colleague telling me about this research seemed to think I was being a bit of an asshole, but Im used to it.

First, we have to consider the central hypothesis that there is a fitness cost associated with human males not being sure of paternity. Obviously, raising children takes a bazillion resources so from that perspective a dad doesn't want to waste his time and energy raising Chet's kid. That explanation jives with our sense of selves in our current society, but what about 4000 years ago? Prehistorically (and historically for most of the planet) people lived as hunter-gatherers, in family units. Not being an expert in anthropology (maybe Dr. Laden will comment if he sees this post), but my understanding is that a given male in the tribe spends less time raising one specific child. Resources are acquired and distributed amongst the members, fucking socialists. So under most of human evolution, what were the selective pressures that would promote the behaviors the authors take as givens?

Even today, while there are reasons to want to ensure paternity, if paternity were a major part of male behavioral make up, presumably we would all have a dozen mistresses on the side to maximize our chances to get some paternity. Of course, while we were visiting our mistresses, our mates could use that time to help the local studmuffin with his paternity issues.

Basically, I don't like these behavioral rationales because it is trivial to argue them any way you like. We could look at the animal kingdom to gain some potential insights, but that's a clusterfuck as well. Chimpanzees, gorillas, and bonobos all have extremely different sexual behaviors. Lions kill their step children, eagles mate for life, cuckoos force surrogates, seahorse males exclusively care for the young, penguins mate for a season raise a chick then trade up or at least out. So whatever human behavior you want to rationalize, there will be an example in the animal kingdom you can use.

Modified from paper
Ok, so let's take the behavioral rationales off the table and simply look at what the authors did. One thing they wanted to test was the semen displacement hypothesis. What? You don't know what the semen displacement hypothesis is? Well, its the idea that the shape of the penis allows it to act like a scoop to remove another dudes semen if said other dude recently had sex with the woman you were currently copulating with.

The authors acquired some artificial penises (commonly known as dildos) and an artificial vagina (commonly referred to as damned if I know) and made artificial semen (cornstarch and water). The authors put the "semen" in the "vagina" and then "copulated" using the "penis". (If ever a sentence needed scare-quotes.) Then the amount of "semen" remaining was then measured to come up with the following data set.

These are the phallus types

So both dildo penis B and D, which have scoops displaced 85-90% of the cornstarch. Whereas  VibroMaxxx penis C displaced 30-40% of the cornstarch. It looks like the hypothesis is supported. However, I have some concerns. First, cornstarch isnt semen. For one thing, semen contains spermatozoa that swim, like towards an egg cell. The authors removed that variable by making the "vagina" a closed orifice. By sealing one end, there's no place for anything else to go but stay still or be pulled out. In the real world, maybe the act of secondary copulation pushes more semen and sperm of the first guy deeper into the vagina closer to the cervix and the ultimate prize the egg. That was not an option here.

Second, where have all the good sperm gone? During ejaculation, the sperm come out with a fair bit of thrust (yes, I know). While much of the semen remains within the vaginal cavity, I wonder how quickly sperm that most likely fertilize an egg leave the vagina? The vaginal cavity is not a hospitable place for sperm. It's essentially a lethal acid bath, not to mention there's mucus that you can get hung up in, and immunological cells acting like you don't belong there. Getting out of Dodge is a good thing. If we take the scooping results presented as solid, the question becomes, in real life what's being scooped out: competing healthy sperm of your best friend or the dead residuals of said ex-best friend?

Third, timing. For this hypothesis to work, it seems like a woman would have to find another mating partner in a reasonably quick period of time. How common is a rapid turn around time? If it isn't that common, there's probably little to no selective advantage because we have to factor in the chance the first guy wins anyway as well as all the times copulations fail to produce a pregnancy.

There was a lot more in the paper, some surveys (YAY!!) and what not. You should read the paper to get all the details. But color me not convinced. The idea the human penis shape plays a role in sexual competition is interesting, but there seems to be too much hand waving to justify the research. If we take these 3-5 things as givens, then.... Well, I'm not a fan of taking things as givens.

I am convinced of one thing though. If during sex, I recall that my penis may have evolved a scoop-like shape to help remove semen from a competitor, it'll probably be time to call it quits.

Interesting aside. In all of this work and study, the woman is completely neutral just a bystander in the process. If there was a penal shape competition going on, I would fully expect that there was also a role for the female in this process, she would not want a sub-par partner ruining her perfectly good plans. Women may promote successful copulations with the primary stud of interest by changing position to allow deeper penetrations during climax for one partner but not the other, for example.

Gallup, G. (2003). The human penis as a semen displacement device Evolution and Human Behavior, 24 (4), 277-289 DOI: 10.1016/S1090-5138(03)00016-3

R01s and Me

R01 grants, the standard grant that runs a lab from NIH, are now scored based on 5 criteria: Significance, Investigator(s), Innovation, Approach, Environment. Each criteria is given a score ranging from 1-10, with 1 being awesome and 10 being death. You really want 1s and 2s across the board have a strong chance at funding.
The best calendars year after year
When proposals are submitted, they go to a study section, which probably has 70-90 proposals to consider. Of these proposals, probably at best 5 will be funded. In order to give the "best" grants more consideration, grants outside a certain a range are not discussed at the study section meeting (why bother talking about #63). These "not discussed" grants are triaged. You get your scores from the study section members that directly reviewed the proposal, but no overall score. Now depending on study section, the grants actually being discussed proposals have 1s, 2s, 3s, 4s, and maybe some 5s.

A couple things to note, the Investigator and Environment scores do not vary much in study sections. Why would they? Presumably the person submitting the grant is a published scientist, generally a faculty member at a university or research center and the environment is where the research is done, university or research center. The one score that seems to matter most and tracks with the "Overall" score is Approach.

I have been submitting a bunch of proposals recently, who hasn't, and thought I'ld share some of my experiences. Now every study section is different and scores/trends in scores can vary markedly, so my experience may not apply to you. I should note that of these proposals, 3 were submitted to the same study section an the other 2 were submitted to different study sections (1 has funded me in the past), but all study sections were within the same Institute of NIH.

Remember the scores are for Significance, Investigator(s), Innovation, Approach, Environment. I have used the code S I I A E to represent  these respectively. So here are the scores for 5 proposals I have submitted recently and you should note that all of these proposals were "Not Discussed" (Yes, it does suck to be me sometimes.)

Grant 1         S  I  I  A  E
Critique 1     3  3  3  4  3
Critique 2     3  2  2  4  2
Critique 3     6  3  6  6  2
(Comment: Fucking reviewer #3)

Grant 2         S  I  I  A  E  (Similar types of analyses as Grants 1 and 5)
Critique 1     7  5  6  8  2
Critique 2     5  2  7  3  1
Critique 3     4  4  6  5  4

(Comment: Environment 4?!?! Apparently Reviewer #3 thinks my major research institution is not all that cut out to do the basic molecular genetics work I have been doing for a decade)

Grant 3        S  I  I  A  E  (Change in research focus, completely different study section)
Critique 1    3  7  8  8  6
Critique 2    6  4  8  7  3
Critique 3    7  4  6  7  4

(Comment: Alright this proposal either sucks or was sent to the completely wrong study section. Actually both possibilities could be true. Check out those Approach scores 8, 7, 7. Charlie Sheen would tell me Im Winning. Regardless, mistakes were made. The amount of time needed to put together an strong R01 proposal in my opinion takes too long to use )

Grant 4        S  I  I  A  E  (Similar types of analyses as Grants 1 and 5)
Critique 1    4  2  3  6  2
Critique 2    3  2  3  4  1
Critique 3    5  2  3  3  2

Grant 5        S  I  I  A  E  (A1 of grant #1 above)
Critique 1    3  2  3  3  1
Critique 2    3  2  3  3  2
Critique 3    5  2  4  4  1
(Comment: Fucking reviewer #3...again. This really sucks because this grant is now considered dead. An A1 proposal, a resubmission, cannot be put back in without major fundamental changes. So here is a grant that is reasonably close to the funding area, but it cannot be honed it must be fundamentally altered. Is this really the best use of my time NIH?)

So Grants #1 and #5 (5 was a resubmission of 1) are close and by my reading missing some Omph in the sales department. I will figure out a way to keep at it with this project (Im looking at you NSF). Grant #4 has another shot, although that 6 and 4 under Approach mean serious work has to be done to beef this one up. Grant #2 needs to go to the study section #1, #4, and #5 went to, looking back I directed it incorrectly. Grant #3 requires another publication, a complete rewrite/focus, and a new study section. I think Grant #3 is dead and will ultimately evolve into Grant #6, 7, 8, or whatever number Im up to by then.

Cells that vomit fungus and other issues of science papers

This weeks
journal club was on Cryptococcus neoformans and an odd way it may get of out macrophage some of the time, at least in vitro, maybe. The paper in question is: 

The Human Fungal Pathogen Cryptococcus neoformans Escapes Macrophages by a Phagosome Emptying Mechanism That Is Inhibited by Arp2/3 Complex-Mediated Actin Polymerisation by Simon A. Johnston, Robin C. May. PLoS Pathogens 6(8) e1001041.

This work follows up a really cool observation published by two groups in back to back articles in Current Biology back in 2006. Basically Cryptococcus neoformans gets into your lungs and can cause pulmonary infections. Macrophage are defensive cells of your body that are essentially cellular Pac-People that go around scarffing up foreign organisms that get into you, like C. neoformans. When I say scarf up, what I mean is the macrophage take up the microbe into a large vesicle called a phagosome, this is like the garbage disposal of the cell. What's important to remember is that the phagosome is separate from the cytoplasm of the macrophage and is effectively the surrounding environment. Generally macrophage either kill the invader or, in some cases, are killed by it, although a few disease-causing microbes can survive and grow just fine within the macrophage. C. neoformans was one of those microbes that either killed or were killed by macrophage (it is a competition, if things go well the C. neoformans is killed, if things go poorly, the macrophage is killed), or sometimes lived inside macrophage. However, in 2006 two groups published something completely different that is better seen than described.
(link in case it doesn't work for you)
What you are looking at is a big macrophage cell that contains 6-7 small C. neoformans cells within phagosomes. Around minute ~350 you'll notice the number of C. neoformans cells increases (the C. neoformans cells are dividing), and then around minute 540 something subtle happens. You may need to watch it several times to see it. Yep, all the freaking C. neoformans cells are vomited from the macrophage!!! Importantly the macrophage didn't lyse (explode) in the process. In fact, the macrophage is still alive, it divides at minute 740! That is the coolest shit eveh!

I&I 2000 paper Figure 9C. This is part of a single macrophage,
all the white glop is capsule. (The edge of the macrophage
can be seen near the bottom of the figure as the thin curvy white
area. The black box is irrelevant here.) 
Unfortunately, I was not as thrilled by this follow up paper. One big issue is that while the original observation was filled with awesomeness, there was the issue of relevance. This issue can be overlooked in the initial analysis because of the shear awesomeness. The phenomenon may be amazing to see in the laboratory under artificial conditions, but does it matter in real life, in the human host? There is a large body of literature demonstrating the ability of C. neoformans to kill macrophage. This happens by the production of massive amounts of capsule which gums up the macrophage (see figure). So while the initial observation was amazing and worth the publicity, now the question of relevance needs to be addressed.

Sadly, today's paper essentially ignored the question and went right on into determining some of the macrophage requirements for this vomiting phenomenon. I want to discuss a number of concerns that came out of our departmental journal club. (I can not take credit for all of these concerns, but I do agree with them and appreciated the discussions that arose because of them.) You should read the paper for the details as I gloss over many of them below. Plus, there is a tremendous amount of cellular biology in the paper if you are interested in cell biology. 

Concern 1. So what?
From Lab Rat
L. monocytogenes
swimming on actin
I have already noted the relevance issue regarding the phenomenon in question. This paper demonstrates that the macrophage Arp2/3 complex is important for this phenomenon as well. The authors show that actin filaments (one of the internal skeletons of a eukaryotic cell) surround phagosomes containing C. neoformans and that this requires Arp2/3. The Arp2/3 complex is required for formation of virtually all actin filaments in a cell, the notable exception being actin filaments that occur during cytokinesis. Once Arp2/3 was shown to be involved, that basically ends the story. There was no need to kill the horse it rode in on and then start beating it. Don't get me wrong it was important to show Arp2/3 was required. If Arp2/3 was not required, then that would have been interesting in its own right, as that would have been similar to what is seen for Listeria monocytogenesL. monocytogenes, an intracellular bacterial pathogen, uses host cell actin to move around and shoot itself into neighboring cells. (While much of  L. monocytogenes motility is Arp2/3-dependent, there is Arp2/3-independent motility as well.)

Ok, once we know Arp2/3 is required, so what? It is well known that actin filaments require Arp2/3. Actin filaments also require the degradation of previously generated filament (to recycle the actin monomers) and even translation of the mRNA encoding actin. What have we actually learned here? What's the new important finding?

Concern 2. Please deal with contradictions.
In the first paragraph of the results, if you say "Long term time lapse imaging over 18 hours revealed that phagosomes containing cryptococci showed rapid, transient increases in actin-GFP fluorescence...that appeared similar to actin flashes previously macrophages loaded with latex beads [16]. " then please remember it four sentences later when you say "Notably, flashes were extremely rare on phagosomes containing latex beads (either unopsonised or IgG-opsonised) (Figure 1D)." Doesn't this seem like a discrepancy that needs to be addressed? 

Also, the results suggest that the more actin "flashes" that occur the more likely vomiting will occur (Figure 3A and B). Based on this, the prediction I would make is that drugs that promote filament formation would promote vomiting; drugs that inhibit filament formation would inhibit vomiting. Well the results of the drug experiments (Figure 4) reveal completely different data. Not a big deal, but I would expect an explanation, which was absent. (If the authors had different predictions that these results agreed with, it was not apparent to me.)

Finally, the idea the authors propose is that the phagosomal membrane gets leaky, which is why actin filaments form there. This is tested using dextran blue, a large molecular polymer of glucose linked to a blue dye. Dextran blue is taken up by macrophage along with  C. neoformans and located within the phagosome with the C. neoformans. If the phagosome becomes leaky, one expects the dextran blue to be in the cytoplasm. Well, the dextran blue does separate from the C. neoformans but it is not diffuse in the cytoplasm. The dextran blue is found in punctate spots (Figure 5), which I think could be vesicles that have separated from the major phagosome. If someone has better insights than myself, post them in the comments.

Concern 3. Philosophy of Science.
Science, at least the biological sciences, is usually based in hypothesis testing although there is a fair bit of observational science as well. When we discuss of findings, like in the discussion part of the paper, we put out our favorite ideas for what is happening (favorite ≠ best, necessarily). We sell our stuff to make it interesting to the largest audience possible. But, we also consider the limitations to our favorite ideas and even consider other possible explanations, even if we discount them shortly thereafter. We do this in writing. We do this as part of the process of being critical thinkers. I saw no evidence of this in the paper. The discussion flew right down the road of we think this, and it means that, yadda, yadda, yadda until we reach the Methods and Materials section. Part of this lack may have been due to point #1 So What? The authors may have been trying to avoid this issue being raised.

Concern 4. Conflict of interests.
Personally, I thought this work, which was labor intensive, was still quite preliminary. The data presented was generally well done, but there were a fair number of holes that, in my opinion, needed to be filled in to justify the conclusions being made. That is not to say that this paper needed any additional ducks in a row to be published. However, this paper was published in PLoS Pathogens, one of the premier journals dealing with pathogens and disease, so more ducks would be helpful. I was a little surprised...and then I saw this "One of the authors (RCM) is an editor for PLoS Pathogens". On the positive side, this is laid out clearly at the beginning of the paper as a potential conflict of interest. But I cannot help but wonder if there is some unconscious bias when one of the editors for a journal submits their paper to said journal. Yes, the manuscript was handled by a different journal editor, but these people do work together to strengthen the journal and make it successful. Do you really want to shit on a colleague who's a member of your team? I'll point out that I would not be eligible to even review a paper submitted to PLoS Pathogens if the author were also a faculty member at my university (note there are ~1500 faculty members at my university). 

Overall the paper is dealing with an interesting phenomenon, but I do think its time to determine if the phenomenon is biologically relevant. It may be possible to identify C. neoformans mutants that get vomited more or less often. If such mutants can be identified, you can see how these mutants behave in the host, which may clue you in on if/how this vomiting phenomenon contributes to colonization/infection.

(For the record, I have had a couple of papers rejected from PLoS Pathogens, which constitutes my own potential bias.)

Johnston SA, & May RC (2010). The human fungal pathogen Cryptococcus neoformans escapes macrophages by a phagosome emptying mechanism that is inhibited by Arp2/3 complex-mediated actin polymerisation. PLoS pathogens, 6 (8) PMID: 20714349

How Bacteria Swim in Your Stomach

ResearchBlogging.orgWe started our Microbiology Journal Club of the new year, technically a new decade. We started off with a bang, well a bang from a physics perspective, more of a whimper from a microbiology perspective.

The paper under discussion was:

Helicobacter pylori moves through mucus by reducing mucin viscoelasticity. by Celli JP et al. Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14321-6.

The basic premise is that H. pylori, a spiral shaped bacteria is thought to burrow its way through the gastric mucus, like a cork screw to get to the underlying epithelial cells lining your stomach. However, this work suggests another mechanism. But let's back up a little.

H. pylori - Yutaka Tsutsumi, MD

How do the epithelial cells lining your stomach survive? Great question, Im glad you asked. The epithelial cells secrete several things to protect themselves one of which is mucus. Gastric mucus has an amazing property of being able to change its viscosity. Kind of like molasses is watery when heated and almost solid when cooled. There is no decision making going on by the mucus, this is strictly a property of physics and chemistry. Now gastric mucus is interesting because it is more 'solid' the lower the pH, like 2, and more 'liquid' at higher pH, like 7. What this means is that where the mucus is exposed to acid it forms a protective shell, but closer to the epithelial cells, it is less viscous.

What does this have to do with H. pylori? Another great question. I should point out that H. pylori does not grow at pH 2, its killed by this environment much like most everything else. 
H. pylori actually modifies the local pH through an enzyme called urease that generates ammonia, which has a pH of around 12. Pretty good way to deal with stomach acid. Ill also point out that H. pylori mutants that cannot make urease are absolutely killed in the stomach. So the idea has been that H. pylori makes urease until it can burrow through the mucus to get to the epithelial cells where the pH is much more conducive to life.

But how does H. pylori burrow through the mucus when it is like a shell? That is the $64,000 question and the one considered by the authors of the paper. Remember that the viscosity of the mucus is affected by pH and that H. pylori can make the local environment less acidic. This led to the hypothesis that H. pylori increases the pH (making it less acidic), which also reduces the viscosity of the mucus (its easier to swim through) and that's how H. pylori gets through the mucus to the epithelial cells. The authors then did a number of studies to support their hypothesis, although did little to rule it out. In fact one the disappointments is that important controls were essentially non-existant and the authors could have had a much tighter more informative study if they had done them. (I should point out the paper was published in the "Biophysics and computational biology" section of PNAS not the "Microbiology" section.)

One of the first experiments done is to compare gastric mucus at pH 4 (control) with gastric mucus + H. pylori (which quickly becomes pH 7). There are two variables here, does everyone see them? The first, the one the authors care about is the presence/absence of bacteria. The second is pH. So when I see data like in Figure 1 (1B is shown), I have thoughts. 

This panel is showing the nonlinear viscoelastic response of the samples, don't worry I don't know what that means either. Regardless, the white lines, no bacteria pH 4 samples, are constant (flat) until the applied stress reaches ~10 Pa, and then they drop like a rock. The red lines, + bacteria pH 7 samples, show a different response. So the authors conclusion is that the bacteria have an effect, which I agree with. However, I want to see the data for the no bacteria pH 7 experiment (not done) or the + bacteria pH 4 experiment (not done. This latter experiment could easily be done by simply using the urease mutant, which does not increase the pH). These experiments would demonstrate whether the difference in viscoelasticity was due ONLY to the pH effect caused by the bacteria or due to the pH effect and additional effects. These bacteria also secrete proteases that could degrade the mucus, which would also reduce the viscosity.

The authors include some movies and pictures of cells and also measure some things in these datasets. However, it is really impossible to determine what is being measured or how cells were chosen. For example, one movie uses mucus at pH 4 (without urea, so the bacteria cannot change the pH) and the one bacterium shown tries real hard to swim, but doesn't go far (were there any others?). The other movie uses mucus at pH 6 and a number of bacteria, three of which move around quite well, the others do not move much at all. So when the authors are mapping the movement of bacteria (Figure 2) did they simply ignore the cells not moving? do a different experiment? what? I can't tell.

Regardless, I think the authors are on to something. I do not believe they have thrown out the burrowing model described previously. But I do believe they have refined it and made it more biologically meaningful. By looking at the true nature of gastric mucus and thinking about the bacteria in this context, I think the authors have gained some biological insights into what these bacteria need to do to survive and how the gastric mucus protects us (from acid, already known, and maybe from other bacteria, not previously known at least not via this mechanism).

Finally, I thought this work suggested something else. The model being used is that the bacteria get into your stomach, don't ask how you don't really want to know how your GI tract is colonized. The stomach is a hostile environment and the bacteria have a short time to get to safety by the epithelial cells. The bacteria secrete a bucketload of urease, increase the pH to survive a bit longer and also to reduce the viscosity of the mucus so they can swim through it to safety. Once there, the bacteria can cause chronic inflammation, which damages the epithelial cells, and can eventually lead to gastric cancer.

I suggest another possibility. The bacteria usually get in to us as infants when our stomach pH is not a acidic as it is when we are older. The bacteria survive long enough to colonize our stomachs and things go on there merry way. If the bacteria grow too much, there is sufficient reduction in the local viscosity of the mucus that acid can leak through and damage the epithelial cells (remember they don't like it either). Damage leads to inflammation and chronic damage can cause ulcers to form and eventually cancer.

These two ideas are not mutually exclusive and there is still the question why do some people get gastric illness from H. pylori and others do not.

Celli, J., Turner, B., Afdhal, N., Keates, S., Ghiran, I., Kelly, C., Ewoldt, R., McKinley, G., So, P., Erramilli, S., & Bansil, R. (2009). Helicobacter pylori moves through mucus by reducing mucin viscoelasticity Proceedings of the National Academy of Sciences, 106 (34), 14321-14326 DOI: 10.1073/pnas.0903438106

Woman who caused Earthquake interviewed tomorrow

Jen McCreight of Blaghag fame will be on Atheist Talk tomorrow (Sunday) March 13th 9AM Central on AM 950. McCreight became more infamous by starting Boobquake. When an Islamic cleric blames earthquakes on women wearing immodest clothing (he should have seen the French Canadian on the Maine beaches in the late 70s!), the Jen McCreights of the world test the hypothesis. Of course a 6.5 magnitude earthquake did occur concomitant with boobquake, so call in and ask her to defend her actions against humanity.

Also, the discussion will address the following: 

"Why are women more religious than men when most
religions are so anti-woman? Jen McCreight will address this paradox,
make the case for why it’s time for women to leave religion, and
discuss why skepticism and atheism are empowering for women. "

You can live stream the show, simply enter a Minnesota zip code, like 55455.

AbC Turned 4

WOW, I was thinking it is about that time of year...Indeed, on the first of this month 4 years ago I published my first post. I have been vomiting opinion thoughts and ideas sporadically ever sense. Since AbC's inception, I have published 187 posts and have averaged ~50 posts a year.

The big change this last year was joining "Field of Science " which, not surprisingly, has increased traffic. (Although I still haven't come close to repeating my peak hits in a day of >6000 after PZ linked to a post of mine.) Its been fun being part of a collective and reading the work of other interesting science minded people.

Happy belated birthday to my blog. Hope this year will be even better than last.

Further thoughts on sex

Go here , buy their stuff!!!
Fellow blogger LabRat commented on a recent post where I, in part, point out the problem with sexual reproduction and discount the answer generally given to this problem. Because I am a competitive jerk, I am going to use LabRat's comment as a stepping stone to make a few general points, because I think they highlights some misconceptions or at least unsubstantiated ideas in biology. (LabRat's comments are in red, like the kid to the right, my responses are in awesome, aka the Magium kid!)

1. You need sex if you have a nucleus.
No you don't. I realize this makes for a simply dichotomy that LabRat uses to contrast in the next sentence, but it is not correct. First, this ignores the basic problem, which is why is there sex. If nucleus makes sex essential (need), then there should not be asexual eukaryotes, but there are. Many of them in fact and many that are sister species to eukaryotes that still have sexual reproduction. BTW don't forget whiptail lizards (I will beat on them like a dead horse).

2. If you don't, gaining genetic diversity is very, *very* easy you can just pick up random genes from anywhere and try them out.
There are two assumptions in this statement that I want to call into question. The first assumption is that the nucleus is the barrier to picking up random DNA from the environment (which is the idea I think LabRat was making). Is that true? If it is, that means eukaryotic cells still take up DNA from the environment just fine (it is a great source of nutrients) but cannot get the DNA into the nucleus. My experience in eukaryotic genetics suggests this isn't true. Simply making cells more permeable is sufficient to get DNA into the nucleus, which means the nucleus isn't the issue.

The second assumption is that bacteria can easily take up DNA from the environment. In the case of Vibrio cholerae that is true, if they're growing on a crab shell (freely available article). I think LabRat is highlighting the importance and sexiness of Horizontal Gene Transfer (HGT). HGT clearly occurs between bacteria, not just different cells of the same species, but also different species, hell even different phyla! It is a phenomenon built of WIN! and really HGT was a game changer for how we (scientists) think about biology. HGT is important and its discovery revolutionized bacterial genetics. But let's not overstate it. HGT has occurred and is important. But is it a potential force of evolution? Yes. Is it the driving force? No, well at least not necessarily. In fact, bacterial species have a way to generate genetic diversity without taking up DNA from the environment, which is based on DNA polymerase IV. DNA polymerase IV is an error prone DNA polymerase, which means when replicating the DNA of a bacterium it makes more mistakes than other DNA polymerases. This results in a bunch of additional mutations. This is not generally a good thing, but DNA pol IV is only expressed when things are bad for the bacterium. If you're in the process of dying anyway, generating a bunch of mutations will help you on your way or may actually result in something happening that lets you survive. 

3. Once you package all the DNA away though you need to have all sorts of random twisted 'crossing over' and specialised sharing-DNA events in order to get any kind of diversity in your genome.
From here. Compare CAI-4 and WO-1
"all sorts of random twisted 'crossing over' and specialised sharing-DNA events' is long hand for sexual reproduction. However, I want to point out that there is only one reason why you want diversity in your genome, and that is to get phenotypic diversity. One can have an extremely stable genetic repertoire in a population (clones) and still get lots of phenotypic diversity. One word: Epigenetics. Also, one does not need a mating partner to get structural changes in the genome. One of my favorite organisms, Candida albicans, frequently, on the order of 10% of clinical isolates, has rearranged genomes, see figure.

4. And the risks of no genetic diversity at all are far too high.

Maybe, but this is a hypothesis. An almost certainly absolutely correct hypothesis in most circumstances, but still a hypothesis. However, I want to stress that genetic diversity is meaningless except as a proxy for phenotypic diversity and as I noted above there are many ways to generate phenotypic diversity independent of genetic diversity. Further, genetic diversity can be generated in the absence of sex.

Finally I will close with my last rejoinder to why I do not think the current explanations for the evolution of sexual reproduction are sufficient.

Right Wing Pundits Befuddle Amurikans on DOMA

A few days ago on Talk of the Nation the discussion was on Obama's decision to no longer defend the DOMA law in court. The discussion was fairly standard stuff and Nina Totenberg did an excellent job laying out the situation.

Thankfully, we have a political party that either doesn't understand the constitution or ignores it in order to enrage the base. This party does not seem to know that there is a difference between enforcing a law (the job of the executive branch) and defending a law in court (not the job of the executive branch, although often the executive branch does this job).

19:38 Matt from Clarksville Tennessee demonstrates the problem perfectly. Matt has picked up on the talking points of his masters. See how long it takes Matt to finally get it through his thick head that the issue is not enforcement not defense (23:59). But even then, Matt is still going to be righteously indignant about a problem that doesn't exist.

Sadly, someone who I expect has a similar viewpoint as me comes on next, and then basically says the president does not need to follow the law. The wrongness in her follow up comments helps reinforce my belief that >95% of US born citizens would probably fail the tests immigrants take to obtain citizenship.

101 Dalmatians, Not an Animal Rights Documentary

Look I realize that reality currently has a liberal bias and that sucks for some of the conservatives. Hell, four decades ago reality had a conservative bias and it sucked for some of the liberals. The difference between then and now is that if you want to have someone affirm you wrongness, you can simply turn on the TV and find the information you want, and I do mean want. Many Americans are not turning on the TV to get information, but to simply have their preconceived notions reaffirmed, which they are then calling information.

Not a documentary about the fur industry
Case in point, if you watch FOX news for any reason other than pornographic entertainment you are likely an idiot. Regardless what you get from this station will bring nothing to the conversation/discussion at hand. Its not that you have a conservative, small government, pro-business philosophy which is nauseating. Its that you use fiction not as an allegory or metaphor but as reality. Its like PETA using "101 Dalmatians" as a case study in animal cruelty. Anyone with any sense at all realizes that FOX news is propaganda lock stock and barrel. It is a mouthpiece of George Soros Richard Murdock.

Now all news outlets make mistakes. Its a fact. No argument. But no news outlet makes the number of 'mistakes' that FOX news makes, nor do any other news outlets make all their mistakes in a one dimensional fashion (in a proconservative manner).

For example, there is a significant protest happening in Wisconsin in response to the proposed union busting of governor Walker (R - duh). It has been all over the news.

FOX news even decided to cover it and came up with the following:

1. First apparently the neighboring state, which is at the same latitude, ends winter sometime in January/early February. Or FOX news lies (the key is the lack of snow and all the greenery on those non-evergreens not to mention the clothing of people standing around outside in ~15-20°F weather).

2. Second, apparently FOX news has a problem cutting and pasting numbers or figures from one source to their own database. (On a mac, its Command-C followed by Command-V; on a PC its right-click select copy followed by right-click select paste)

3. Third, apparently if a protestor touches someone working for FOX news and the person who touched you gets harangued by other protestors, well that's assault and you were punched and got charlie horses, but of course despite the beating you were so macho (and dare I say a ladies man) that you just dealt with it.

(As an aside, I believe the beaten and pummeled reporter (it got better) is being interviewed by 'We-never-use-Nazi-analogies' Megyn Kelley.)

FOX news has been a propaganda machine for many years, but the point has been reached (was reached about 15 years ago) where a line in the sand was crossed. If FOX news is your source of 'information' then as far as I am concerned your opinions thoughts etc do not matter. You have chosen to not be part of the discussion. I'ld seat you at the kids table, but the kids are so well behaved and decent, I wouldn't want you teaching them your bad habits.

H/T Stephanie Zvan

Another thing not getting done soon

Cleaned and organized 5 bookshelves this weekend and set aside those books I either still need to read or finish reading. I put them in a pile, which became two piles. Sigh.

The odd thing is I will still be buying books this year regardless of how quickly I move through this pile. Indeed the third and fourth book down in the left pile were belated birthday presents to myself from a week ago.