de novo origin of genes

Kathy sent me a link to a recent paper in Science describing the appearance of new genes in Drosophila.

“Until recently, de novo origin of genes was considered to be so unlikely as to be impossible,” comparative genomicist Aoife McLysaght of the Smurfit Institute of Genetics at Trinity College in Dublin, Ireland, who was not involved in the study, told The Scientist in an e-mail. “[T]his population level analysis is important because it gives a new insight into the very early stages of the origin and establishment of genes de novo.”

This is pretty exciting stuff. Here's a link to a report in The Scientist and you'll find the Science paper citation there.

Natural History of Nitrogen Fixation

I think this paper, the Natural History of Nitrogen Fixation, provides most of the answers I was looking for - but then it raises further questions.

It has been suggested that abiotic sources of fixed nitrogen on the early Earth, supplied through endogenous/abiotic synthesis and exogenous delivery, were most likely limiting (Raven and Yin 1998; Kasting and Siefert 2001; Navarro-Gonzalez, McKay, and Mvondo 2001). At some point, dwindling concentrations of reduced nitrogen would have become insufficient for an expanding microbial biomass, precipitating the evolution of biological nitrogen fixation (Towe 2002). These prevailing conditions have been used to argue that the innovation of biological nitrogen fixation occurred early in prokaryotic evolution, and indeed the ability to fix nitrogen is found exclusively among members of the bacteria and archaea.

So usable nitrogen probably was limiting to early microbes. But questions remain about how such an expensive and complex metabolic process evolved.

We explore the complex genetic history of the nitrogenase family, which is replete with gene duplication, recruitment, fusion, and horizontal gene transfer and discuss these events in light of the hypothesized presence of nitrogenase in the last common ancestor of modern organisms, as well as the additional possibility that nitrogen fixation might have evolved later, perhaps in methanogenic archaea, and was subsequently transferred into the bacterial domain.

Pollination syndromes (or not)

A bee that's not following the rules. For an explanation see 'Bees use achromatic contrast to see red.'

‘Pollination syndromes’ are suites of phenotypic traits reflecting convergent adaptations of flowers for pollination by specific types of animals. It's easy to find examples that fit the theory but are the syndromes testable?

In a 2009 paper in Annals of Botany Jeff Ollerton and colleagues use flowers from six communities on three continents and score them for the expression of floral traits used in published descriptions of the pollination syndromes. They then compare these to the actual pollinators.

Bottom line:

(I)n approximately two-thirds of plant species, the most common pollinator could not be successfully predicted by assuming that each plant species belongs to the syndrome closest to it in phenotype space.

Haplodiploidy

Also in Science this week: Why Queens Prefer Daughters A comment on a recent paper in the American Naturalist that investigates the relationship between sociality, sex ratio adjustment and haplodiploidy.

Hamilton’s “haplodiploidy hypothesis” holds that inflated sororal relatedness has promoted altruistic sib rearing in haplodiploids, potentially explaining their apparent predisposition to eusociality. Here, we suggest that haplodiploidy may instead promote eusociality simply by facilitating sex-ratio adjustment. Specifically, haplodiploidy may enable sex-ratio bias toward the more helpful sex, owing to “local resource enhancement,” and such sex-ratio bias may promote the evolution of helping by individuals of that sex, owing to the “rarer-sex effect.” This could explain why haplodiploidy appears to have been important for eusociality in taxa with only female helpers, such as ants, wasps, and bees, but not in taxa with both male and female helpers, such as termites.

Interspecies signalling

In the journal Cell this week (with this neat 'graphical abstract'):
Bacterial Nitric Oxide Extends the Lifespan of C. elegans

Nitric oxide (NO) is an important signaling molecule in multicellular organisms. Most animals produce NO from L-arginine via a family of dedicated enzymes known as NO synthases (NOSes). A rare exception is the roundworm Caenorhabditis elegans, which lacks its own NOS. However, in its natural environment, C. elegans feeds on Bacilli that possess functional NOS. Here, we demonstrate that bacterially derived NO enhances C. elegans longevity and stress resistance via a defined group of genes that function under the dual control of HSF-1 and DAF-16 transcription factors. Our work provides an example of interspecies signaling by a small molecule and illustrates the lifelong value of commensal bacteria to their host.

Science Daily has a report as well: Nitric Oxide: A Little Molecule's Remarkable Feat -- Prolonging Life, Worm Study Shows
Nitric oxide, the versatile gas that helps increase blood flow, transmit nerve signals, and regulate immune function, appears to perform one more biological feat -- prolonging the life of an organism and fortifying it against environmental stress, according to a new study.

Nitric oxide is why all the cool kids, well the athletic ones anyway, are drinking beet juice. Beet juice has large amounts of nitrate which bacteria in you mouth and intestines convert to nitrites which is converted to nitric oxide. This lowers blood pressure and increases oxygen supply to tissues: All the Olympic Athletes Are Guzzling Beet Juice. The only downsides are that beet juice is an acquired taste (although beet-carrot-apple is pretty good), and that it colors your urine a disturbing bright red.

Donor feces

I've been reading a lot about clinical trials lately. The press tend to make too much out of small effects that may not mean very much and a great many of our drugs, even well known and very popular ones, are little better than a placebo.

In any double-blind clinical trial the results are monitored by an outside body to ensure, for example, that any dangerous side-effect of the drug or treatment, is noticed and the trial can be stopped. In rare instances they also decide the drug, or treatment, is so successful that they also stop the trial so that everyone can benefit. When they do this it's usually a good sign the researchers are onto something big.

That's what happened in one of the first clinical trials of fecal transplants published last month in the New England Journal of Medicine:
Duodenal Infusion of Donor Feces for Recurrent Clostridium difficile

There's a description of the issue and the research at Wired's Superbug blog. They link to an NPR article that describes the work of a Canadian team to come up with synthetic feces called RePOOPulate.

Insect Astronomers

Not really relevant to anything we are talking about right now but I thought this was cool and that some of you might enjoy it.

Lowly Dung Beetles Are Insect Astronomers

Even the humble dung beetle, its life spent barely an inch above the ground, pushing balls of waste, steers by starlight.

This unsuspected navigational mechanism, described Jan. 24 in Current Biology, is likely not limited to the Scarabaeus satyrus examined by the researchers.

Peering through compound eyes into the darkness of night, insects around the world may be guided by stars.

Arsenic Life Redux

Nov. 29, 2010. NASA announces a news conference "to discuss an astrobiology finding that will impact the search for evidence of extraterrestrial life."

If you don't remember this then read the story as it unfolded here: The Arsenic Chronicles
A humble arsenic-friendly microbe from Mono Lake, Calif., has recently stirred a tempest in the science world's teapot. Here's the story as it played out over the last two weeks in tweets, blogs and news conferences, of course.

Now, with that background, you may enjoy this article from USA Today a few days ago:
Glowing reviews on 'arseniclife' spurred NASA's embrace
USA Today reporters got hold of Science's reviews of the original article via a Freedom of Information Request.

Pace says there was "poor judgment at multiple levels" in the arseniclife case, from an "overly exuberant" interpretation of the study results by the authors to the peer reviewers missing "the big crux of the results: the claim of absence of phosphorus," to NASA repeating some of the mistakes that caused the agency trouble in 1996, when it publicized results suggesting a Martian meteorite contained microscopic signs of life. 

Spirit Bears

A white mother Spirit bear and a black cub offspring; the father must have been black and the cub is a heterozygote for the coat color polymorphism. This picture really reminds me of the old Polar Bear joke which is not really suitable for printing here...

It's Carl Zimmer again with a really nice practical example of one of the simulations we will look at in class tomorrow - the interplay between genetic drift and natural selection: Snow Coyotes and Spirit Bears

The Bear part of the story is based on this paper in the journal 'Evolution': POPULATION GENETICS OF THE WHITE-PHASED “SPIRIT” BLACK BEAR OF BRITISH COLUMBIA

The Spirit (or Kermode) bear is a white-phased black bear found on the northwest coast of British Columbia, and is one of the most striking color polymorphisms found in mammals. A single nucleotide polymorphism at the melanocortin 1 receptor gene (mc1r) locus is the cause of this recessive w variant. Recently, evidence suggests that the white color provides a selective advantage during salmon hunting. Here we examine the effects of favorable selection, gene flow, genetic drift, and positive-assortative mating in an effort to understand the establishment and maintenance of this polymorphism and the observed heterozygote deficiency for mc1r but not for microsatellite loci. It appears that genetic drift was important in the establishment of the w allele and that the selective advantage was important to counteract immigration from populations without the w allele. Positive-assortative mating can result in a deficiency of heterozygotes but needs to be quite high to result in the large deficiency of heterozygotes observed, suggesting that other factors must also be contributing. Examination of population genetic factors, singly and jointly, provides insight into the establishment and maintenance of this unusual polymorphism.

Epigenetic news

A paper in Nature this week, Germline DNA Demethylation Dynamics and Imprint Erasure Through 5-Hydroxymethylcytosine, provides important details for how epigenetic information could be inherited.

From the ScienceDaily report:

Dr Jamie Hackett from the University of Cambridge, who led the research, said: "Our research demonstrates how genes could retain some memory of their past experiences, revealing that one of the big barriers to the theory of epigenetic inheritance -- that epigenetic information is erased between generations -- should be reassessed."

...

"However, it is not yet clear what consequences, if any, epigenetic inheritance might have in humans. Further studies should give us a clearer understanding of the extent to which heritable traits can be derived from epigenetic inheritance, and not just from genes. That could have profound consequences for future generations."

Blood falls

Blood Alley, Blood Diamond, Blood Red, Blood Simple, Blood Ties, Blood Work, Bloodbrothers, Bloodfist, Bloodline, Bloodsport.

Huh, apparently no-one has ever made a movie called Blood Falls.

The Blood Falls story, that is pictured in your textbook, is highlighted in a news report at the NSF website: Unusual Antarctic Microbes Live Life on a Previously Unsuspected Edge.

The News report was inspired by an article in Science entitled: A Contemporary Microbially Maintained Subglacial Ferrous "Ocean"

An active microbial assemblage cycles sulfur in a sulfate-rich, ancient marine brine beneath Taylor Glacier, an outlet glacier of the East Antarctic Ice Sheet, with Fe(III) serving as the terminal electron acceptor. Isotopic measurements of sulfate, water, carbonate, and ferrous iron and functional gene analyses of adenosine 5′-phosphosulfate reductase imply that a microbial consortium facilitates a catalytic sulfur cycle. These metabolic pathways result from a limited organic carbon supply because of the absence of contemporary photosynthesis, yielding a subglacial ferrous brine that is anoxic but not sulfidic. Coupled biogeochemical processes below the glacier enable subglacial microbes to grow in extended isolation, demonstrating how analogous organic-starved systems, such as Neoproterozoic oceans, accumulated Fe(II) despite the presence of an active sulfur cycle.

86 million year old lunch box

In a tenuous link to the previous posts on obesity I was drawn to the following news article on NPR:
Ancient Deep-Sea Bacteria Are In No Hurry To Eat

The Science paper the report is based on isn't quite as catchy:
Aerobic Microbial Respiration in 86-Million-Year-Old Deep-Sea Red Clay

 but the observations and the implications are pretty interesting:

They left the surface 86 million years ago with one lunch box, and they're still eating out of it. It's like they're splitting a pie, and they keep splitting in half and in half and in half, but nobody ever eats the last crumble. It's quite remarkable.
... 
One reason scientists are interested in this extreme lifestyle is because it provides clues about the absolute minimum conditions required to sustain life. Andreas Teske, a marine microbiologist at the University of North Carolina, Chapel Hill, says that's useful for people looking beyond our planet for signs of life.

Causes of obesity - part 2

Well if you did your homework and watched the HBO shows you heard quite a bit about fatty liver disease and saw some fatty. I haven't watched the last two shows yet but, so far, there's been no mention of an intriguing new hypothesis that obesity and fatty liver disease in particular may be infectious and therefore treatable with antibiotics. This is not a new suggestion but some of the best evidence to date, from studies of mice, was published in February in Nature:

Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity

"When healthy mice were co-housed with mice that had altered gut microbes, the healthy mice also developed a susceptibility for development of liver disease and obesity."

A number of newspapers and blogs picked up on this fairly dramatic result. Here's part of a blog posting by Suzanne O'Malley at the Huffington Post:

New findings suggest that obesity and liver disease can be caused by proteins that change microbe populations in the stomach, according to a study published in the February 2012 issue of the journal Nature. The Yale immunobiologists' discovery suggests that obesity and non-alcoholic fatty liver disease (NAFLD) may be infectious and treatable with targeted antibiotics. At least that was the case for mice. NAFLD is caused by metabolic syndrome -- diabetes, hypertension, and high blood cholesterol -- which are also risk factors for heart disease. Researchers expanded on an earlier study that showed microbial imbalances in the stomach, caused by the same family of proteins, heightened the risk of intestinal diseases such as colitis. The most extraordinary finding, according to senior author Richard A. Flavell, a Howard Hughes Medical Institute investigator and professor of immunobiology at Yale School of Medicine, was that the changed intestinal environment that led to obesity and liver disease was infectious among the community of mice studied.
 ...
The next step, Flavell says, is extending this research to humans and identifying more precisely the bacteria involved in the progression to liver disease.

How do muscles contract?

I spent a bit too long on immunology and ran out of time to cover muscles. Check out section 48.1 and 48.2 in your textbook which cover this quite clearly.

Note though that this 'sliding filament' model of muscle contraction was only discovered in the 1950's. The key evidence used to construct the model was a series of electron micrographs like those to the right of the picture.

You textbook does a nice job of interpreting the micrographs (figs 48.1 and 48.2) in the context of the theory but it's interesting to consider if you only had the pictures do you think you would have come up with the correct model?

The sliding filament model was actually proposed by two groups working independently and their papers were published together in the same issue of Nature.

 Structural changes in muscle during contraction: interference microscopy of living muscle fibres

Changes in the cross-striations of muscle during contraction and stretch and their structural interpretation 
 
In 2004 Nature published a special focus to celebrate the papers and look at progress in the subsequent decades on 'one of the most intriguing of biological problems: that of the conversion of chemical energy to mechanical work'.

Multiple pollen tubes

Going back to last quarter but I thought this paper in Current Biology this month was interesting: Gamete Fusion Is Required to Block Multiple Pollen Tubes from Entering an Arabidopsis Ovule

Plants need to make sure that their female gametes are fertilized but they also need to make sure that only two fertile sperm reach the ovule.

When gamete fusion fails, one of two pollen tube-attracting synergid cells persists, enabling the ovule to attract more pollen tubes for successful fertilization. This mechanism prevents the delivery of more than one pair of sperm to an ovule, provides a means of salvaging fertilization in ovules that have received defective sperm, and ensures maximum reproductive success by distributing pollen tubes to all ovules.

Not dying sooner

Some confusing headlines this week on the effect of coffee drinking on health.

Most newspapers went with some variation of 'Coffee drinkers live longer', but the truth was a little more complex than that.

The research, published this week in the New England Journal of Medicine, Association of Coffee Drinking with Total and Cause-Specific Mortality, actually reached a slightly different conclusion:
In this large prospective study, coffee consumption was inversely associated with total and cause-specific mortality. Whether this was a causal or associational finding cannot be determined from our data. 

The Washington Post, who have some good science reporters, did well with No, drinking coffee probably won’t make you live longer
The study’s researchers found that coffee drinkers were more prone to engage in a whole host of unhealthy activities. They smoke more, are more likely to consume three or more alcoholic drinks a day and eat more red meat. They exercise less and eat fewer fruits and vegetables.
When the researchers isolated coffee consumption as a single variable, they did indeed see a drop in the risk of premature death. But when they looked at coffee-drinkers who had those bad health habits, the risk of death was actually higher: Coffee-drinkers are actually more likely to die early because of those habits.

and BoingBoing got all wrapped up with Coffee associated with the opposite of death, according to new scientific study
I think what they're trying to tell us is that while drinking coffee does not necessarily cause you to live longer, it is associated with the opposite of dying sooner.

I'll just note that for maximum 'not dyingness' you need to drink six or more cups a day....

Suicide-bags

Suicide-bags would probably be a good name for a band. If this was the 1970's. Suicide-bags is also a name for the lysosomes found within cells because as well as pathogen destruction they are involved in the natural process of cell organelle recycling and even cell death. This degradation and recycling of ageing and dying cells, or autophagy, is attracting a lot of attention these days because of its links to disease and aging.

The science writter Carl Zimmer wrote an article for the New York Times on this topic, Self-Destructive Behavior in Cells May Hold Key to a Longer Life based on a paper in Trends in Cell Biology: The regulation of aging: does autophagy underlie longevity?
Recent evidence has revealed that autophagic activity is required for lifespan extension in various long-lived mutant organisms, and that numerous autophagy-related genes or proteins are directly regulated by longevity pathways. These findings support the emerging view that autophagy is a central regulatory mechanism for aging in diverse eukaryotic species.

A billion heartbeats

One reason I love California is that you can exercise here without being considered weird. In many parts of the country (and world) the active exerciser is considered as a threat to the lifestyle of the sedentary who will go to considerable lengths to explain how exercise is actually bad for you. I have had people stop beside me at traffic lights and lean out of their windows to explain the damage I am doing to my knees by running (not true by the way). But my favorite is the constant heartbeat theory.

This idea is actually quite old - one paper suggests it came to prominence in the late 1800's industrial revolution with the observation that machines that ran fast wore out more quickly. It then became 'supported' by observations across species - bigger animals live longer and also have lower heart rates. Perhaps we all have a finite number of heartbeats and exercising will only use them up faster. Oh noes. However even if this were true (which it isn't) it would not be an argument against exercise because one consequence of being fit is a lower resting heart rate. You don't need to lower it much to have the reduced beats in the 22-23 hours a day you aren't exercising more than compensate for the hour or two you do.

Although the initial theory proposed a constant number of heart beats this became refined to suggest that it's the speed at which an organism processes oxygen that matters. There is evidence, when comparing species, that creatures with faster oxygen metabolisms die younger. Tiny mammals with rapid heartbeats metabolize oxygen quickly and have short lifespans. Tortoises, on the other hand, metabolize oxygen very slowly and have long lifespans. The free-radical theory of ageing provides a potential mechanism that links metabolism to ageing phenomena, since oxygen free radicals are formed as a by-product of oxidative phosphorylation.

The debate rumbles on. One of the complexities is that even if a relationship exists between species we wouldn't necessarily expect it to be the same within a species. When we look within a species it gets very complicated. here's a summary from a 2005 paper in the Journal of Experimental Biology  (Body size, energy metabolism and lifespan):
The observed patterns of association between rates of energy metabolism and the rates of ageing (or lifespans) of animals within species include all the potential patterns of association - positive, negative and not significant. 

Obesity epidemic

We haven't started our physiology section yet but with today's dramatic headlines from the CDC's 'Weight of the Nation' event I thought I'd post a little about obesity.

Obesity is not simply being overweight, it's usually defined as having a Body Mass Index over 30. To put this in perspective I weigh 160lb and have a BMI pretty much in the middle of the normal range. If I put on 70lbs of weight (which would be about two Otto's worth - Otto is the 30+lb cat in the picture who has since lost weight) I would still not be obese (although I would be overweight!) So obesity is not simply a medical term for being overweight - it is a precise medical term for being VERY overweight. We know that at this point obesity causes many serious health problems.

Now in today's headlines we see the shocking news that 36% of American's are now obese (up from 12% in 1990 and 22% in 2000) and by 2030 that is estimated to rise to 42% leading to somewhere around half a TRILLION dollars in extra healthcare costs between now and then (compared to if obesity rates stayed at 2010 levels). This is all based on a paper in the American Journal of Preventive Medicine - Obesity and Severe Obesity Forecasts Through 2030.
About the only good news is that the paper actually results in a lower estimate of future obesity than some previous analyses but that's cold comfort given the conclusions:

The study estimates a 33% increase in obesity prevalence and a 130% increase in severe obesity prevalence over the next 2 decades. If these forecasts prove accurate, this will further hinder efforts for healthcare cost containment.

The paper also provides some estimates for 'severe obesity' (BMI>40 - for me that would be just about doubling my weight to 310lb). These estimates are actually worse than current estimates. By 2030 they predict that 10% of the US population will be severely obese.

ATP parasite

I haven't quite digested this yet but this paper from 2008 describes a Eukaryote that has lost its mitochondria - as I briefly mentioned in class. In this case though the remnant mitochondria, known as a mitosome, actually consumes ATP - that the host cell must absorb from its host. Reversing the usual relationship between mitochondria/mitosome and host cell. Funky.

Thus, uniquely among eukaryotes, the traditional relationship between mitochondrion and host has been subverted in E. cuniculi, by reductive evolution and analogous gene replacement. Instead of the mitosome providing the parasite cytosol with ATP, the parasite cytosol now seems to provide ATP for the organelle.