13 research outputs found
Population genomics of marine zooplankton
Author Posting. © The Author(s), 2017. This is the author's version of the work. It is posted here for personal use, not for redistribution. The definitive version was published in Bucklin, Ann et al. "Population Genomics of Marine Zooplankton." Population Genomics: Marine Organisms. Ed. Om P. Rajora and Marjorie Oleksiak. Springer, 2018. doi:10.1007/13836_2017_9.The exceptionally large population size and cosmopolitan biogeographic distribution that
distinguish many â but not all â marine zooplankton species generate similarly exceptional patterns of
population genetic and genomic diversity and structure. The phylogenetic diversity of zooplankton has
slowed the application of population genomic approaches, due to lack of genomic resources for closelyrelated
species and diversity of genomic architecture, including highly-replicated genomes of many
crustaceans. Use of numerous genomic markers, especially single nucleotide polymorphisms (SNPs), is
transforming our ability to analyze population genetics and connectivity of marine zooplankton, and
providing new understanding and different answers than earlier analyses, which typically used
mitochondrial DNA and microsatellite markers. Population genomic approaches have confirmed that,
despite high dispersal potential, many zooplankton species exhibit genetic structuring among geographic
populations, especially at large ocean-basin scales, and have revealed patterns and pathways of population
connectivity that do not always track ocean circulation. Genomic and transcriptomic resources are
critically needed to allow further examination of micro-evolution and local adaptation, including
identification of genes that show evidence of selection. These new tools will also enable further
examination of the significance of small-scale genetic heterogeneity of marine zooplankton, to
discriminate genetic ânoiseâ in large and patchy populations from local adaptation to environmental
conditions and change.Support was provided by the
US National Science Foundation to AB and RJO (PLR-1044982) and to RJO (MCB-1613856); support to
IS and MC was provided by Nord University (Norway)
Dynamic EBV gene loads in renal, hepatic, and cardiothoracic transplant recipients as determined by real-time PCR light cycler
Corticotropin-releasing factor receptors in the dorsal raphe nucleus modulate social behavior in Syrian hamsters
An investigation of novice ESL writersâ cognitive processes and strategy use of paraphrasing
Development and psychometric properties of the Y-PASS questionnaire to assess correlates of lunchtime and after-school physical activity in children
Toward Understanding How Early-Life Stress Reprograms Cognitive and Emotional Brain Networks
Vulnerability to emotional disorders including depression derives from interactions between genes and environment, especially during sensitive developmental periods. Adverse early-life experiences provoke the release and modify the expression of several stress mediators and neurotransmitters within specific brain regions. The interaction of these mediators with developing neurons and neuronal networks may lead to long-lasting structural and functional alterations associated with cognitive and emotional consequences. Although a vast body of work has linked quantitative and qualitative aspects of stress to adolescent and adult outcomes, a number of questions are unclear. What distinguishes ânormal' from pathologic or toxic stress? How are the effects of stress transformed into structural and functional changes in individual neurons and neuronal networks? Which ones are affected? We review these questions in the context of established and emerging studies. We introduce a novel concept regarding the origin of toxic early-life stress, stating that it may derive from specific patterns of environmental signals, especially those derived from the mother or caretaker. Fragmented and unpredictable patterns of maternal care behaviors induce a profound chronic stress. The aberrant patterns and rhythms of early-life sensory input might also directly and adversely influence the maturation of cognitive and emotional brain circuits, in analogy to visual and auditory brain systems. Thus, unpredictable, stress-provoking early-life experiences may influence adolescent cognitive and emotional outcomes by disrupting the maturation of the underlying brain networks. Comprehensive approaches and multiple levels of analysis are required to probe the protean consequences of early-life adversity on the developing brain. These involve integrated human and animal-model studies, and approaches ranging from in vivo imaging to novel neuroanatomical, molecular, epigenomic, and computational methodologies. Because early-life adversity is a powerful determinant of subsequent vulnerabilities to emotional and cognitive pathologies, understanding the underlying processes will have profound implications for the world's current and future children