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New and Exciting in PLoS ONE

There are 32 new articles on PLoS ONE this week. Here are some titles that caught my eye – go read, rate, annotate and comment:

Why Men Matter: Mating Patterns Drive Evolution of Human Lifespan:

Evolutionary theory predicts that senescence, a decline in survival rates with age, is the consequence of stronger selection on alleles that affect fertility or mortality earlier rather than later in life. Hamilton quantified this argument by showing that a rare mutation reducing survival is opposed by a selective force that declines with age over reproductive life. He used a female-only demographic model, predicting that female menopause at age ca. 50 yrs should be followed by a sharp increase in mortality, a “wall of death.” Human lives obviously do not display such a wall. Explanations of the evolution of lifespan beyond the age of female menopause have proven difficult to describe as explicit genetic models. Here we argue that the inclusion of males and mating patterns extends Hamilton’s theory and predicts the pattern of human senescence. We analyze a general two-sex model to show that selection favors survival for as long as men reproduce. Male fertility can only result from matings with fertile females, and we present a range of data showing that males much older than 50 yrs have substantial realized fertility through matings with younger females, a pattern that was likely typical among early humans. Thus old-age male fertility provides a selective force against autosomal deleterious mutations at ages far past female menopause with no sharp upper age limit, eliminating the wall of death. Our findings illustrate the evolutionary importance of males and mating preferences, and show that one-sex demographic models are insufficient to describe the forces that shape human senescence.

Phylogenomics Reshuffles the Eukaryotic Supergroups:

Resolving the phylogenetic relationships between eukaryotes is an ongoing challenge of evolutionary biology. In recent years, the accumulation of molecular data led to a new evolutionary understanding, in which all eukaryotic diversity has been classified into five or six supergroups. Yet, the composition of these large assemblages and their relationships remain controversial.

Here, we report the sequencing of expressed sequence tags (ESTs) for two species belonging to the supergroup Rhizaria and present the analysis of a unique dataset combining 29908 amino acid positions and an extensive taxa sampling made of 49 mainly unicellular species representative of all supergroups. Our results show a very robust relationship between Rhizaria and two main clades of the supergroup chromalveolates: stramenopiles and alveolates. We confirm the existence of consistent affinities between assemblages that were thought to belong to different supergroups of eukaryotes, thus not sharing a close evolutionary history.

This well supported phylogeny has important consequences for our understanding of the evolutionary history of eukaryotes. In particular, it questions a single red algal origin of the chlorophyll-c containing plastids among the chromalveolates. We propose the abbreviated name ‘SAR’ (Stramenopiles+Alveolates+Rhizaria) to accommodate this new super assemblage of eukaryotes, which comprises the largest diversity of unicellular eukaryotes.

Quadrupling Muscle Mass in Mice by Targeting TGF-ß Signaling Pathways:

Myostatin is a transforming growth factor-ß family member that normally acts to limit skeletal muscle growth. Mice genetically engineered to lack myostatin activity have about twice the amount of muscle mass throughout the body, and similar effects are seen in cattle, sheep, dogs, and a human with naturally occurring loss-of-function mutations in the myostatin gene. Hence, there is considerable interest in developing agents capable of inhibiting myostatin activity for both agricultural and human therapeutic applications. We previously showed that the myostatin binding protein, follistatin, can induce dramatic increases in muscle mass when overexpressed as a transgene in mice. In order to determine whether this effect of follistatin results solely from inhibition of myostatin activity, I analyzed the effect of this transgene in myostatin-null mice. Mstn−/− mice carrying a follistatin transgene had about four times the muscle mass of wild type mice, demonstrating the existence of other regulators of muscle mass with similar activity to myostatin. The greatest effect on muscle mass was observed in offspring of mothers homozygous for the Mstn mutation, raising the possibility that either myostatin itself or a downstream regulator may normally be transferred from the maternal to fetal circulations. These findings demonstrate that the capacity for increasing muscle growth by manipulating TGF-ß signaling pathways is much more extensive than previously appreciated and suggest that muscle mass may be controlled at least in part by a systemic mode of action of myostatin.

Insights from Amphioxus into the Evolution of Vertebrate Cartilage:

Central to the story of vertebrate evolution is the origin of the vertebrate head, a problem difficult to approach using paleontology and comparative morphology due to a lack of unambiguous intermediate forms. Embryologically, much of the vertebrate head is derived from two ectodermal tissues, the neural crest and cranial placodes. Recent work in protochordates suggests the first chordates possessed migratory neural tube cells with some features of neural crest cells. However, it is unclear how and when these cells acquired the ability to form cellular cartilage, a cell type unique to vertebrates. It has been variously proposed that the neural crest acquired chondrogenic ability by recruiting proto-chondrogenic gene programs deployed in the neural tube, pharynx, and notochord. To test these hypotheses we examined the expression of 11 amphioxus orthologs of genes involved in neural crest chondrogenesis. Consistent with cellular cartilage as a vertebrate novelty, we find that no single amphioxus tissue co-expresses all or most of these genes. However, most are variously co-expressed in mesodermal derivatives. Our results suggest that neural crest-derived cartilage evolved by serial cooption of genes which functioned primitively in mesoderm.

The Antibacterial Protein Lysozyme Identified as the Termite Egg Recognition Pheromone:

Social insects rely heavily on pheromone communication to maintain their sociality. Egg protection is one of the most fundamental social behaviours in social insects. The recent discovery of the termite-egg mimicking fungus ‘termite-ball’ and subsequent studies on termite egg protection behaviour have shown that termites can be manipulated by using the termite egg recognition pheromone (TERP), which strongly evokes the egg-carrying and -grooming behaviours of workers. Despite the great scientific and economic importance, TERP has not been identified because of practical difficulties. Herein we identified the antibacterial protein lysozyme as the TERP.

Corpus Callosum Morphology in Capuchin Monkeys Is Influenced by Sex and Handedness:

Sex differences have been reported in both overall corpus callosum area and its regional subdivisions in humans. Some have suggested this reflects a unique adaptation in humans, as similar sex differences in corpus callosum morphology have not been reported in any other species of primate examined to date. Furthermore, an association between various measurements of corpus callosum morphology and handedness has been found in humans and chimpanzees. In the current study, we report measurements of corpus callosum cross-sectional area from midsagittal MR images collected in vivo from 14 adult capuchin monkeys, 9 of which were also characterized for hand preference on a coordinated bimanual task. Adult females were found to have a significantly larger corpus callosum: brain volume ratio, rostral body, posterior midbody, isthmus, and splenium than adult males. Left-handed individuals had a larger relative overall corpus callosum area than did right-handed individuals. Additionally, a significant sex and handedness interaction was found for anterior midbody, with right-handed males having a significantly smaller area than right-handed females. These results suggest that sex and handedness influences on corpus callosum morphology are not restricted to Homo sapiens.

Simple Sequence Repeats Provide a Substrate for Phenotypic Variation in the Neurospora crassa Circadian Clock:

WHITE COLLAR-1 (WC-1) mediates interactions between the circadian clock and the environment by acting as both a core clock component and as a blue light photoreceptor in Neurospora crassa. Loss of the amino-terminal polyglutamine (NpolyQ) domain in WC-1 results in an arrhythmic circadian clock; this data is consistent with this simple sequence repeat (SSR) being essential for clock function.

Since SSRs are often polymorphic in length across natural populations, we reasoned that investigating natural variation of the WC-1 NpolyQ may provide insight into its role in the circadian clock. We observed significant phenotypic variation in the period, phase and temperature compensation of circadian regulated asexual conidiation across 143 N. crassa accessions. In addition to the NpolyQ, we identified two other simple sequence repeats in WC-1. The sizes of all three WC-1 SSRs correlated with polymorphisms in other clock genes, latitude and circadian period length. Furthermore, in a cross between two N. crassa accessions, the WC-1 NpolyQ co-segregated with period length.

Natural variation of the WC-1 NpolyQ suggests a mechanism by which period length can be varied and selected for by the local environment that does not deleteriously affect WC-1 activity. Understanding natural variation in the N. crassa circadian clock will facilitate an understanding of how fungi exploit their environments.

Comments

  1. #1 Scott Belyea
    August 29, 2007

    I suggest that neither your blog nor the links you give do an acceptable job of explaining to the new reader what the cutesy “acronym” PLoS ONE (as you write it) or PLoS one (as the page titles at the links write it) is all about. Yes, I can burrow my way around and find out, but why make it frustrating?

    And a question – is the ONE an acronym? I gave up looking around for an explanation of what it meant.

    The PLoS pages are nicely done. Why not make it easier for the new reader to get acquainted? Unexplained acronyms (especially in every page title) are an unnecessary annoyance …

  2. #2 coturnix
    August 29, 2007

    Well, I can’t do that in every PLoS post I make, can I? Every day? Most of my readers know very well what PLoS is and what PLoS ONE is. But OK, here it is:

    PLoS stands for Public Library of Science. ONE is not an acronym, but suggests that “all the good science is in ONE place” (i.e., not that it is the #1 journal, as some suggested it means).

  3. #3 Scott Belyea
    August 29, 2007

    Well, I can’t do that in every PLoS post I make, can I? Every day?

    Tweak your bio …

    “I am the Online Community Manager at PLoS-ONE (Public Library of Science).” And make “Public Library of Science” a link to http://www.plos.org/.

    Or put the PloS logo image and a link at the bottom of your bio.

    Or put something similar at the top of the right sidebar.

    Most of my readers know very well what PLoS is and what PLoS ONE is.

    And if you’re content to leave it at that, carry on … just trying to help …

  4. #4 Bill
    August 29, 2007

    Well, I can’t do that in every PLoS post I make, can I? Every day?

    Sure you can — and since it’s your job to bring *new* readers to the PLoS community I think Scott has a good point. I can think of at least two ways to do it: link PLoS ONE to the same page (an explanation of the name) every time you use it, or simply add a brief explanation as a P.S. to the bottom of each PLoS ONE post. (I like the link better myself.)

  5. #5 Bill
    August 29, 2007

    Heh. Scott and I cross-posted.

  6. #6 coturnix
    August 29, 2007

    OK, this is much more constructive advice. I will do something like this shortly. Sorry for short blogger’s temper earlier- I was in the middle of an off-blog crisis at the time.

  7. #7 Bill
    August 29, 2007

    I will do something like this shortly.

    Sweet.

    I have a post in mind comparing different publishers’ responses to online comments and criticism — think about the difference between this conversation and, say, Shelley’s experience with Wiley.

    Hope the meatspace crisis is over.

  8. #8 Stagyar zil Doggo
    August 30, 2007

    Thus old-age male fertility provides a selective force against autosomal deleterious mutations at ages far past female menopause with no sharp upper age limit, eliminating the wall of death.

    If I’m reading this correctly, it sez that tis the dirty old men lusting after (and mating with) barely legal girls that keeps women from dying immediately after menopause. Wow! Who’d have thunk that?

    The implication also seems to be (and I barely passed high school biology, so please be gentle in correcting me if I’m wrong) that if such a deleterious mutation showed up in the mitochondrial genome, we would all be doomed to die at 51. Do the authors offer any explanations for why that hasn’t already occured?

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