Phenotypic Plasticity & Evolution

Phenotypic plasticity – the ability of an individual organism to alter its features in direct response to a change in its environment – is ubiquitous. Understanding how and why this phenomenon exists is crucial because it unites all levels of biological inquiry. This book brings together researchers who approach plasticity from diverse perspectives to explore new ideas and recent findings about the causes and consequences of plasticity. Contributors also discuss such controversial topics as how plasticity shapes ecological and evolutionary processes; whether specific plastic responses can be passed to offspring; and whether plasticity has left an important imprint on the history of life. Importantly, each chapter highlights key questions for future research. Drawing on numerous studies of plasticity in natural populations of plants and animals, this book aims to foster greater appreciation for this important, but frequently misunderstood phenomenon. Key Features Written in an accessible style with numerous illustrations, including many in color Reviews the history of the study of plasticity, including Darwin’s views Most chapters conclude with recommendations for future researc

Moving toward a system genetics view of disease

Testing hundreds of thousands of DNA markers in human, mouse, and other species for association to complex traits like disease is now a reality. However, information on how variations in DNA impact complex physiologic processes flows through transcriptional and other molecular networks. In other words, DNA variations impact complex diseases through the perturbations they cause to transcriptional and other biological networks, and these molecular phenotypes are intermediate to clinically defined disease. Because it is also now possible to monitor transcript levels in a comprehensive fashion, integrating DNA variation, transcription, and phenotypic data has the potential to enhance identification of the associations between DNA variation and diseases like obesity and diabetes, as well as characterize those parts of the molecular networks that drive these diseases. Toward that end, we review methods for integrating expression quantitative trait loci (eQTLs), gene expression, and clinical data to infer causal relationships among gene expression traits and between expression and clinical traits. We further describe methods to integrate these data in a more comprehensive manner by constructing coexpression gene networks that leverage pairwise gene interaction data to represent more general relationships. To infer gene networks that capture causal information, we describe a Bayesian algorithm that further integrates eQTLs, expression, and clinical phenotype data to reconstruct whole-gene networks capable of representing causal relationships among genes and traits in the network. These emerging network approaches, aimed at processing high-dimensional biological data by integrating data from multiple sources, represent some of the first steps in statistical genetics to identify multiple genetic perturbations that alter the states of molecular networks and that in turn push systems into disease states. Evolving statistical procedures that operate on networks will be critical to extracting information related to complex phenotypes like disease, as research goes beyond a single-gene focus. The early successes achieved with the methods described herein suggest that these more integrative genomics approaches to dissecting disease traits will significantly enhance the identification of key drivers of disease beyond what could be achieved by genetic association studies alone

A pan-metazoan concept for adult stem cells : the wobbling Penrose landscape

Funding: EU COST action MARISTEM. Grant Number: 16203 Marie Skłodowska-Curie COFUND program ARDRE. Grant Number: 847681 National Research Agency, ANR. Grant Numbers: ANR-15-IDEX-01, ANR-19-PRC United States-Israel Binational Science Foundation. Grant Number: 2015012Adult stem cells (ASCs) in vertebrates and model invertebrates (e.g. Drosophila melanogaster) are typically long-lived, lineage-restricted, clonogenic and quiescent cells with somatic descendants and tissue/organ-restricted activities. Such ASCs are mostly rare, morphologically undifferentiated, and undergo asymmetric cell division. Characterized by ‘stemness’ gene expression, they can regulate tissue/organ homeostasis, repair and regeneration. By contrast, analysis of other animal phyla shows that ASCs emerge at different life stages, present both differentiated and undifferentiated phenotypes, and may possess amoeboid movement. Usually pluri/totipotent, they may express germ-cell markers, but often lack germ-line sequestering, and typically do not reside in discrete niches. ASCs may constitute up to 40% of animal cells, and participate in a range of biological phenomena, from whole-body regeneration, dormancy, and agametic asexual reproduction, to indeterminate growth. They are considered legitimate units of selection. Conceptualizing this divergence, we present an alternative stemness metaphor to the Waddington landscape: the ‘wobbling Penrose’ landscape. Here, totipotent ASCs adopt ascending/descending courses of an ‘Escherian stairwell’, in a lifelong totipotency pathway. ASCs may also travel along lower stemness echelons to reach fully differentiated states. However, from any starting state, cells can change their stemness status, underscoring their dynamic cellular potencies. Thus, vertebrate ASCs may reflect just one metazoan ASC archetype.Publisher PDFPeer reviewe

9th Annual Postdoctoral Science Symposium

The mission of the Annual Postdoctoral Science Symposium (APSS) is to provide a platform for talented postdoctoral fellows throughout the Texas Medical Center to present their work to a wider audience. The MD Anderson Postdoctoral Association convened its inaugural Annual Postdoctoral Science Symposium (APSS) on August 4, 2011. The APSS provides a professional venue for postdoctoral scientists to develop, clarify, and refine their research as a result of formal reviews and critiques of faculty and other postdoctoral scientists. Additionally, attendees discuss current research on a broad range of subjects while promoting academic interactions and enrichment and developing new collaborations

Evolution of the Hox gene fushi tarazu in arthropods

Homeotic (Hox) genes are important in determining regional identity in virtually all metazoans,and are conserved throughout the animal kingdom. In Drosophila melanogaster, fushi tarazu (ftz) is located within the Hox complex and contains a Hox-like DNA-binding homeodomain, but functions as a pair-rule segmentation gene. At some point(s) during evolution, ftz has undergone three specific changes thought to contribute to its new segmentation function in Drosophila: 1) The gain of an LXXLL motif allowed for interaction with a new co-factor, Ftz-F1; 2) The degeneration of the YPWM motif decreased the ability to interact with the homeotic co-factor Exd; 3) ftz expression switched from Hox-like to seven stripes in Drosophila. Here I isolated ftz sequences and examined expression from arthropods spanning 550 million years of evolutionary time to track these changes in ftz. I found that while the LXXLL motif required for segmentation was stably acquired at the base of the holometabolous insects, the YPWM motif degenerated independently many times in arthropod lineages, and these `degen-YPWMs' vary in their homeotic potential. Additionally, ftz expression in a crustacean is in a weak Hox-like pattern, suggesting a model in which different ftz variants could arise in nature and not be detrimental to organismal development. Given my findings that ftz sequence and expression is so dynamic, I investigated the features that may be preventing ftz fossilization in arthropod genomes. I tested the hypothesis that a broadly conserved role of ftz in the developing central nervous system (CNS) retains ftz in arthropod genomes. This model predicts that the homeodomain, but not variable co-factor interaction motifs, is required for Ftz CNS function. Evidence supporting this model was obtained from CNS-specific rescue experiments in Drosophila. Additionally I examined the expression and function of ftz and ftz-f1 in the short-germ beetle Tribolium castaneum. I found that both genes are expressed in pair-rule patterns, and preliminary results suggest that ftz-f1 is important for proper segmentation and cuticle deposition, and ftz function may be partially redundant with ftz-f1. Taken together, these findings show that variation of a pleiotropic transcription factor is more extensive than previously imagined, and suggest that evolutionary plasticity may be widespread among regulatory genes

Non-genetic Transgenerational Inheritance of Acquired Traits in Drosophila

It is increasingly recognized that acquired traits may be transgenerationally transmitted through non-DNA sequence-based elements, with epigenetics as perhaps the most important mechanism. Here we review examples of non-genetic transgenerational inheritance in Drosophila, highlighting transgenerational programming of metabolic status and longevity, one particular histone modification as an evolutionarily conserved underlying mechanism, and important implications of such studies in understanding health and diseases