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Studying th. genetic basis of speciation in h.gh.gene flow marine invertebrates

Current Zoology 2016年第6期62卷 643-653页

作者： grant h. pogson Department of Ecology and Evolutionary Biology University of California Santa Cruz CA 95064 USA

A growing number of genes responsible for reproductive incompatibilities between species （barrier loci） exh.bit th. signals of positive selection. h.wever, th. possibility th.t genes experiencing positive selection diverge early in speciation and commonly cause reproductive incompatibilities h.s not been systematically investigated on a genome-wide scale. h.re, I outline a research.program for studying th. genetic basis of speciation in broadcast spawning marine invertebrates th.t uses a priori genome-wide information on a large, unbiased sample of genes tested for positive selection. A targeted sequence capture approach.is proposed th.t scores single-nucleotide polymorph.sms （SNPs） in widely separated species populations at an early stage of allopatric divergence. Th. targeted capture of both.coding and non-coding sequences enables SNPs to be ch.racterized at known locations across th. genome and at genes with.known selective or neutral h.stories. Th. neutral coding and non-coding SNPs provide robust background distributions for identifying Fsm-outliers with.n genes th.t can, in principle, identify specific mutations experiencing diversifying selection. If natural h.bridization occurs between species, th. neutral coding and noncoding SNPs can provide a neutral admixture model for genomic clines analyses aimed at finding genes exh.biting strong blocks to introgression. Strongylocentrotid sea urch.ns are used as a model system to outline th. approach.but it can be used for any group th.t h.s a complete reference genome available.

关键词： barrier loci Bobzh.nsky-Muller incompatibilities FsToutliers genome scan introgression positive selection sequence capture speciation.

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h.stone Acetylation, VERNALIZATION INSENSITIVE 3, FLOWERING LOCUS C, and th. Vernalization Response

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Molecular Plant 2009年第4期2卷 724-737页

作者： Donna M. Bond Elizabeth.S. Dennis Barry J. pogson E. Jean Finnegan CSIRO Plant Industry Canberra Australia ARC Centre of Excellence in Plant Energy Biology School of Biochemistry and Molecular Biology Australian National University Canberra Australia

Th. quantitative induction of VIN3 by low temperatures is required for PRC2 repression of FLC and promotion of flowering （vernalization） in Arabidopsis. h.stone acetylation, a ch.omatin modification commonly associated with.gene transcription, increased on VIN3 ch.omatin in two spatially and temporally distinct ph.ses in response to low temperatures. During sh.rt-term cold exposure, h.stone h. acetylation at th. transcription start site rapidly increased, implying th.t it is required for VlN3 induction. Subsequent ch.nges in h.stone h. and h. acetylation occurred following continued VIN3 transcription during prolonged cold exposure. Members of th. SAGA-like transcriptional adaptor complex, including th. h.stone acetyltransferase GCNS, wh.ch.induces expression of th. cold acclimation path.ay genes, do not regulate VlN3 induction during cold exposure, indicating th.t th. cold acclimation path.ay and th. cold-induction of VlN3 are regulated by different transcriptional mech.nisms. Mutations in th. oth.r 11 h.stone acetyltransferase genes did not affect VlN3 induction. h.wever, nicotinamide, a h.stone deacetyiase inh.bitor, induced VIN3 and altered h.stone acetylation at th. VIN3 locus. VIN3 induction was proportional to th. length.of nicotinamide treatment, wh.ch.was associated with.an early-flowering ph.notype and repression of FLC. h.wever, unlike vernalization, th. repression of FLC was independent of VIN3 activity. Nicotinamide treatment did not cause a ch.nge in th. expression of any genes in th. autonomous path.ay or members of th. PRC2 complex, th. well ch.racterized repressors of FLC. Our data suggest th.t FLC is repressed via a novel path.ay involving th. SIR2 class of h.stone deacetylases.

关键词： Cold acclimation h.stone acetyltransferase h.stone deacetylase SIR2 nicotinamide.

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