The Genetic Basis of a Rare Flower Color Polymorphism in Mimulus lewisii Provides Insight into the Repeatability of Evolution

A long-standing question in evolutionary biology asks whether the genetic changes contributing to phenotypic evolution are predictable. Here, we identify a genetic change associated with segregating variation in flower color within a population of Mimulus lewisii. To determine whether these types of changes are predictable, we combined this information with data from other species to investigate whether the spectrum of mutations affecting flower color transitions differs based on the evolutionary time-scale since divergence. We used classic genetic techniques, along with gene expression and population genetic approaches, to identify the putative, loss-of-function mutation that generates rare, white flowers instead of the common, pink color in M. lewisii. We found that a frameshift mutation in an anthocyanin pathway gene is responsible for the white-flowered polymorphism found in this population of M. lewisii. Comparison of our results with data from other species reveals a broader spectrum of flower color mutations segregating within populations relative to those that fix between populations. These results suggest that the genetic basis of fixed differences in flower color may be predictable, but that for segregating variation is not.     

Diverse aerobic anoxygenic phototrophs synthesize bacteriochlorophyll in oligotrophic rather than copiotrophic conditions,suggesting ecological niche

While investigating aerobic anoxygenic phototrophs (AAP) from Lake Winnipeg's bacterial community, over 500 isolates were obtained. Relatives of 20 different species were examined simultaneously, identifying conditions for optimal growth or pigment production to determine features that may unify this group of phototrophs. All were distributed among assorted α-Proteobacterial families including Erythrobacteraceae, Sphingomonadaceae, Sphingosinicellaceae, Acetobacteraceae, Methylobacteriaceae, and Rhodobacteraceae. Major phenotypic characteristics matched phylogenetic association, including pigmentation, morphology, metal transformations, tolerances, lipid configurations, and enzyme activities, which distinctly separated each taxonomic family. While varying pH and temperature had a limited independent impact on pigment production, bacteriochlorophyll synthesis was distinctly promoted under low nutrient conditions, whereas copiotrophy repressed its production but enhanced carotenoid yield. New AAP diversity was also reported by revealing strains related to non-phototrophic Rubellimicrobium and Sphingorhabdus, as well as spread throughout Roseomonas, Sphingomonas, and Methylobacterium/Methylorubrum, which previously only had a few known photosynthetic members. This study exemplified the overwhelming diversity of AAP in a single aquatic environment, confirming cultivation continues to be of importance in microbial ecology to discover functionality in both new and previously reported cohorts of bacteria as specific laboratory conditions were required to promote aerobic bacteriochlorophyll production.     

Description of the data from the Collaborative Study on the Genetics of Alcoholism (COGA) and single-nucleotide polymorphism genotyping for Genetic Analysis Workshop 14

The data provided to the Genetic Analysis Workshop 14 (GAW 14) was the result of a collaboration among several different groups, catalyzed by Elizabeth Pugh from The Center for Inherited Disease Research (CIDR) and the organizers of GAW 14, Jean MacCluer and Laura Almasy. The DNA, phenotypic characterization, and microsatellite genomic survey were provided by the Collaborative Study on the Genetics of Alcoholism (COGA), a nine-site national collaboration funded by the National Institute of Alcohol and Alcoholism (NIAAA) and the National Institute of Drug Abuse (NIDA) with the overarching goal of identifying and characterizing genes that affect the susceptibility to develop alcohol dependence and related phenotypes. CIDR, Affymetrix, and Illumina provided single-nucleotide polymorphism genotyping of a large subset of the COGA subjects. This article briefly describes the dataset that was provided.     

Niger’s Child Survival Success,Contributing Factors and Challenges to Sustainability: A Retrospective Analysis

BackgroundHousehold surveys undertaken in Niger since 1998 have revealed steady declines in under-5 mortality which have placed the country ‘on track’ to reach the fourth Millennium Development goal (MDG). This paper explores Niger’s mortality and health coverage data for children under-5 years of age up to 2012 to describe trends in high impact interventions and the resulting impact on childhood deaths averted. The sustainability of these trends are also considered.ConclusionIncreases in access and coverage of care for mothers and children have averted a considerable number of childhood deaths. The 2006 free health care policy and health post expansion were paramount in reducing barriers to care. However the sustainability of this policy and health service provision is precarious in light of persistently high fertility rates, unpredictable GDP growth, a high dependence on donor support and increasing pressures on government funding.     

Insulin and Leptin Signaling Interact in the Mouse Kiss1 Neuron during the Peripubertal Period

Reproduction requires adequate energy stores for parents and offspring to survive. Kiss1 neurons, which are essential for fertility, have the potential to serve as the central sensors of metabolic factors that signal to the reproductive axis the presence of stored calories. Paradoxically, obesity is often accompanied by infertility. Despite excess circulating levels of insulin and leptin, obese individuals exhibit resistance to both metabolic factors in many neuron types. Thus, resistance to insulin or leptin in Kiss1 neurons could lead to infertility. Single deletion of the receptors for either insulin or the adipokine leptin from Kiss1 neurons does not impair adult reproductive dysfunction. However, insulin and leptin signaling pathways may interact in such a way as to obscure their individual functions. We hypothesized that in the presence of genetic or obesity-induced concurrent insulin and leptin resistance, Kiss1 neurons would be unable to maintain reproductive function. We therefore induced a chronic hyperinsulinemic and hyperleptinemic state in mice lacking insulin receptors in Kiss1 neurons through high fat feeding and examined the impact on fertility. In an additional, genetic model, we ablated both leptin and insulin signaling in Kiss1 neurons (IR/LepR^Kiss mice). Counter to our hypothesis, we found that the addition of leptin insensitivity did not alter the reproductive phenotype of IR^Kiss mice. We also found that weight gain, body composition, glucose and insulin tolerance were normal in mice of both genders. Nonetheless, leptin and insulin receptor deletion altered pubertal timing as well as LH and FSH levels in mid-puberty in a reciprocal manner. Our results confirm that Kiss1 neurons do not directly mediate the critical role that insulin and leptin play in reproduction. However, during puberty kisspeptin neurons may experience a critical window of susceptibility to the influence of metabolic factors that can modify the onset of fertility.