Sequential Polygyny During Egg Attendance is Rare in a Tree Frog and Does not Increase Male Fitness

Sequential polygyny is a reproductive strategy that allows males to continue to mate and compensates for the loss of future breeding opportunities incurred by parental care (i.e. egg attendance). Using the frog Kurixalus eiffengeri, we tested predictions that (1) attending males fathered two, overlapping clutches; and (2) that double clutching leads to improved offspring numbers. Using five microsatellite DNA markers, we genotyped 15 pairs of overlapping clutches, which differed slightly in developmental stage at a single egg‐laying site. Parentage analyses showed at least 12 of 15 pairs of overlapping egg clutches were sired by the attending male mated with different females, providing the first genetic evidence to support an earlier prediction that attending males sired both egg clutches. Field surveys found a low incidence of overlapping clutches (4.9% of 263 egg‐occupied stumps), suggesting sequential polygyny is uncommon. Stumps with multiple clutches contained significantly more eggs than stumps with single clutches but hatched similar number of tadpoles. Results suggest that continuous calling that attracts females during egg attendance is a reproductive tactic that maximizes mating opportunities. However, adoption of the sequential polygyny tactic may only result in marginal fitness gains for males that are traded off against average higher egg mortality in larger egg clutches.     

Parental differences in brood provisioning by Hen Harriers Circus cyaneus

Capsule Females varied their provisioning patterns according to brood age and brood size, whereas males did not.

Aims To quantify how parents balance the needs of their offspring for food and protection.

Methods We studied 13 nests from hides and spent on average 101 hours per nest monitoring prey types, provisioning rate and the time spent at the nest by both sexes in relation to brood size and brood age.

Results Males always provided more food than females. Males brought similar amounts of prey items irrespective of brood size and nestling age, whereas females brought more prey and bigger items to larger and older broods. Females spent less time brooding larger broods, particularly early on.

Conclusions Hen Harrier parents share the provisioning burden, with each parent delivering prey as a function of brood care requirements, hunting capability and the behaviour of the other parent.     

TOWARDS A GENERAL THEORY OF GROUP SELECTION

The longstanding debate about the importance of group (multilevel) selection suffers from a lack of formal models that describe explicit selection events at multiple levels. Here, we describe a general class of models for two‐level evolutionary processes which include birth and death events at both levels. The models incorporate the state‐dependent rates at which these events occur. The models come in two closely related forms: (1) a continuous‐time Markov chain, and (2) a partial differential equation (PDE) derived from (1) by taking a limit. We argue that the mathematical structure of this PDE is the same for all models of two‐level population processes, regardless of the kinds of events featured in the model. The mathematical structure of the PDE allows for a simple and unambiguous way to distinguish between individual‐ and group‐level events in any two‐level population model. This distinction, in turn, suggests a new and intuitively appealing way to define group selection in terms of the effects of group‐level events. We illustrate our theory of group selection by applying it to models of the evolution of cooperation and the evolution of simple multicellular organisms, and then demonstrate that this kind of group selection is not mathematically equivalent to individual‐level (kin) selection.     

Structural and biochemical characterization of Rv2140c,a phosphatidylethanolamine-binding protein from Mycobacterium tuberculosis

Rv2140c is one of many conserved Mycobacterium tuberculosis proteins for which no molecular function has been identified. We have determined a high-resolution crystal structure of the Rv2140c gene product, which reveals a dimeric complex that shares strong structural homology with the phosphatidylethanolamine-binding family of proteins. Rv2140c forms low-millimolar interactions with a selection of soluble phosphatidylethanolamine analogs, indicating that it has a role in lipid metabolism. Furthermore, the small molecule locostatin binds to the Rv2140c ligand-binding site and also inhibits the growth of the model organism Mycobacterium smegmatis.     

Mechanical Resistance in Unstructured Proteins

Single-molecule pulling experiments on unstructured proteins linked to neurodegenerative diseases have measured rupture forces comparable to those for stable folded proteins. To investigate the structural mechanisms of this unexpected force resistance, we perform pulling simulations of the amyloid β-peptide (Aβ) and α-synuclein (αS), starting from simulated conformational ensembles for the free monomers. For both proteins, the simulations yield a set of rupture events that agree well with the experimental data. By analyzing the conformations occurring shortly before rupture in each event, we find that the mechanically resistant structures share a common architecture, with similarities to the folds adopted by Aβ and αS in amyloid fibrils. The disease-linked Arctic mutation of Aβ is found to increase the occurrence of highly force-resistant structures. Our study suggests that the high rupture forces observed in Aβ and αS pulling experiments are caused by structures that might have a key role in amyloid formation.     

Mechanical Resistance in Unstructured Proteins

Single-molecule pulling experiments on unstructured proteins linked to neurodegenerative diseases have measured rupture forces comparable to those for stable folded proteins. To investigate the structural mechanisms of this unexpected force resistance, we perform pulling simulations of the amyloid β-peptide (Aβ) and α-synuclein (αS), starting from simulated conformational ensembles for the free monomers. For both proteins, the simulations yield a set of rupture events that agree well with the experimental data. By analyzing the conformations occurring shortly before rupture in each event, we find that the mechanically resistant structures share a common architecture, with similarities to the folds adopted by Aβ and αS in amyloid fibrils. The disease-linked Arctic mutation of Aβ is found to increase the occurrence of highly force-resistant structures. Our study suggests that the high rupture forces observed in Aβ and αS pulling experiments are caused by structures that might have a key role in amyloid formation.     

A dynamic spatiotemporal extracellular matrix facilitates epicardial-mediated vertebrate heart regeneration

Unlike humans, certain adult vertebrates such as newts and zebrafish possess extraordinary abilities to functionally regenerate lost appendages and injured organs, including cardiac muscle. Here, we present new evidence that a remodeled extracellular matrix (ECM) directs cell activities essential for cardiac muscle regeneration. Comprehensive mining of DNA microarrays and Gene Ontology term enrichment analyses for regenerating newt and zebrafish hearts revealed that distinct ECM components and ECM-modifying proteases are among the most significantly enriched genes in response to local injury. In contrast, data analyses for mammalian cardiac injury models indicated that inflammation and metabolic processes are the most significantly activated gene groups. In the regenerating newt heart, we show dynamic spatial and temporal changes in tenascin-C, hyaluronic acid, and fibronectin ECM distribution as early as 3 days postamputation. Linked to distinct matrix remodeling, we demonstrate a myocardium-wide proliferative response and radial migration of progenitor cells. In particular, we report dramatic upregulation of a regeneration-specific matrix in the epicardium that precedes the accumulation and migration of progenitor cells. For the first time, we show that the regenerative ECM component tenascin-C significantly increases newt cardiomyocyte cell cycle reentry in vitro. Thus, the engineering of nature-tested extracellular matrices may provide new strategic opportunities for the enhancement of regenerative responses in mammals.     

Genomic Pathology of SLE-Associated Copy-Number Variation at the FCGR2C/FCGR3B/FCGR2B Locus

Reduced FCGR3B copy number is associated with increased risk of systemic lupus erythematosus (SLE). The five FCGR2/FCGR3 genes are arranged across two highly paralogous genomic segments on chromosome 1q23. Previous studies have suggested mechanisms for structural rearrangements at the FCGR2/FCGR3 locus and have proposed mechanisms whereby altered FCGR3B copy number predisposes to autoimmunity, but the high degree of sequence similarity between paralogous segments has prevented precise definition of the molecular events and their functional consequences. To pursue the genomic pathology associated with FCGR3B copy-number variation, we integrated sequencing data from fosmid and bacterial artificial chromosome clones and sequence-captured DNA from FCGR3B-deleted genomes to establish a detailed map of allelic and paralogous sequence variation across the FCGR2/FCGR3 locus. This analysis identified two highly paralogous 24.5 kb blocks within the FCGR2C/FCGR3B/FCGR2B locus that are devoid of nonpolymorphic paralogous sequence variations and that define the limits of the genomic regions in which nonallelic homologous recombination leads to FCGR2C/FCGR3B copy-number variation. Further, the data showed evidence of swapping of haplotype blocks between these highly paralogous blocks that most likely arose from sequential ancestral recombination events across the region. Functionally, we found by flow cytometry, immunoblotting and cDNA sequencing that individuals with FCGR3B-deleted alleles show ectopic presence of FcγRIIb on natural killer (NK) cells. We conclude that FCGR3B deletion juxtaposes the 5′-regulatory sequences of FCGR2C with the coding sequence of FCGR2B, creating a chimeric gene that results in an ectopic accumulation of FcγRIIb on NK cells and provides an explanation for SLE risk associated with reduced FCGR3B gene copy number.