Newswise — Bethesda, MD—April 30, 2013 – Listed below are the selected highlights for the May 2013 issue of the Genetics Society of America’s journal, GENETICS. The May issue is available online at www.genetics.org/content/current. Please credit GENETICS, Vol. 194, MAY 2013, Copyright © 2013.
Please feel free to forward to colleagues who may be interested in these articles on a wide array of topics including: developmental and behavioral genetics; genome integrity and transmission; genetics of complex traits; cellular genetics; and population and evolutionary genetics.
ISSUE HIGHLIGHTS
Developmental and Behavioral GeneticsAn organelle gatekeeper function for Caenorhabditis elegans UNC-16 (JIP3) at the axon initial segment, pp. 143–161S. L. Edwards, S.-c. Yu, C. M. Hoover, B. C. Phillips, J. E. Richmond, and K. G. MillerNerve cell bodies have a vastly different organelle composition than axons. This article (see accompanying commentary by Zheng and Nonet, pp. 35–37) provides insight into the basis of this difference. The authors report the discovery of a previously unrecognized organelle gatekeeper function, mediated by UNC-16 (JIP3 in humans), that acts at the axon initial segment to restrict the flow of Golgi and endosomal organelles into the synaptic region of axons.
Genome Integrity and TransmissionNovel proteins required for meiotic silencing by unpaired DNA and siRNA generation in Neurospora crassa, pp. 91–100T. M. Hammond, H. Xiao, E. C. Boone, L. M. Decker, S. A. Lee, T. D. Perdue, P. J. Pukkila, and P. K. ShiuandIdentification of small RNAs associated with meiotic silencing by unpaired DNA, pp. 279–284T. M. Hammond, W. G. Spollen, L. M. Decker, S. M. Blake, G. K. Springer, and P. K. ShiuGenes unpaired during meiosis are silenced in Neurospora by a mechanism known as meiotic silencing by unpaired DNA (MSUD). Two articles in this issue of GENETICS report the identification of novel players in this process, including small RNAs and the first nuclear MSUD protein. This protein is not required for meiosis, providing the first indication that MSUD is not necessarily coupled to sexual development. Genome Integrity and TransmissionIntragenomic conflict between the two major knob repeats of maize, pp. 81–89L. B. Kanizay, P. S. Albert, J. A. Birchler, and R. K. DaweLarge genomes are often replete with tandem repeats. Why do they exist? Here the authors investigate the distribution of tandem repeats in maize heterochromatic domains called knobs. The data suggest an intragenomic conflict whereby one family of repeats suppresses proliferation of the other. Similar competition may underlie the formation and maintenance of many tandem repeat arrays.
Genome Integrity and TransmissionNonrandom distribution of interhomolog recombination events induced by breakage of a dicentric chromosome in Saccharomyces cerevisiae, pp. 69–80W. Song, M. Gawel, M. Dominska, P. W. Greenwell, E. Hazkani-Covo, K. Bloom, and T. D. PetesThis article presents the first high-resolution mapping of the positions of chromosome breaks that result from the bridge-fusion-breakage cycles of dicentric chromosomes. Sites of recombination between a dicentric chromosome and its normal homolog revealed the locations of breaks in the dicentric chromosome, which were distributed in a quasi-random fashion between the two centromeres.
Genetics of Complex TraitsSystems genetics of environmental response in the mature wheat embryo, pp. 265–277J. D. Munkvold, D. Laudencia-Chingcuanco, and M. E. SorrellsThis article illustrates the utility of network approaches for understanding gene expression by environment interaction, even in organisms with highly complex genomes. A unique Weighted Gene Co-Expression Network Analysis approach was used to compare gene expression networks in mature wheat embryos from two distinct growing environments across a segregating population. This approach identified environmentally conserved and unique co-expression modules and their genetic control.
Cellular GeneticsThe innate immune response transcription factor Relish is necessary for neurodegeneration in a Drosophila Model of ataxia-telangiectasia, pp. 133–142A. J. Petersen, R. J. Katzenberger, and D. A. WassarmanNeurodegeneration is a hallmark of the human disease ataxia-telangiectasia (A-T), which is caused by mutation of the A-T mutated (ATM) gene. These investigators found that activation of an NF-KB-mediated innate immune response in glial cells causes neurodegeneration in Drosophila ATM mutants. Their finding that Relish, one of the three NF-KB proteins in flies, is necessary for neurodegeneration suggests that neurodegeneration in human A-T is caused by activation of a specific NF-KB protein in glial cells. Population and Evolutionary GeneticsIdentifying loci under selection against gene flow in isolation-with-migration models, pp. 211–233V. M. Sousa, M. Carneiro, N. Ferrand, and J. HeyWhen diverging populations hybridize, regions of the genome near genes associated with population differences or hybrid incompatibilities are prevented from moving from one population to the other. Thus some genes move more freely than others between diverging populations. This article describes a method for estimating rates of gene flow at multiple loci and for identifying loci with reduced gene flow. The authors apply the method to two subspecies of rabbits to show how gene flow can be restricted.Population and Evolutionary GeneticsHigher levels of Neanderthal ancestry in East Asians than in Europeans, pp. 199–209J. D. Wall, M. A. Yang, F. Jay, S. K. Kim, E. Y. Durand, L. S. Stevison, C. Gignoux, A. Woerner, M. F. Hammer, and M. SlatkinNeanderthals occupied most of Europe and parts of Western Asia from 30–300 thousand years ago, and coexisted with modern humans during part of that time. These authors found that modern day East Asians contain on average more Neanderthal DNA than do modern day Europeans. They also show that the East African Maasai contain some Neanderthal ancestry, probably due to recent back-migration of modern humans into Africa.
Genetics of Complex TraitsGenetic dissection of a major anthocyanin QTL contributing to pollinator-mediated reproductive isolation between sister species of Mimulus, pp. 255–263Y.-W. Yuan, J. M. Sagawa, R. C. Young, B. J. Christensen, and H. D. Bradshaw Jr.What underlies prezygotic barriers that lead to reproductive isolation, and ultimately, to speciation? The bumblebee-pollinated Mimulus lewisii and hummingbird-pollinated M. cardinalis are a classic example of pollinator-mediated prezygotic reproductive isolation. These investigators identified an anthocyanin pigment regulatory gene causing a flower color difference that contributes to pollinator preference for each species. This gene is likely to play a role in flower color variation in many other plants.
Cellular GeneticsThe nuclear Argonaute NRDE-3 contributes to transitive RNAi in Caenorhabditis elegans, pp. 117–131J. J. Zhuang, S. A. Banse, and C. P. HunterRNA interference (RNAi) was initially perceived as a cytoplasmic gene silencing process, but genes important for RNAi in C. elegans were found to operate in the nucleus. This article describes unexpected features of one such gene underlying a nuclear RNAi defective (nrde) mutant, which emphasizes the importance of nuclear events during RNAi silencing, especially for transitive RNAi—a mechanism central to RNAi amplification. This Month’s Perspectives
Charles Darwin’s mitochondria, pp. 21–25J. HaymanScholars have long speculated over the nature of Charles Darwin's debilitating illness, with most diagnoses stressing psychogenic roots. In this Perspectives, John Hayman proposes that Darwin suffered from a mitochondrial genetic disease, MELAS syndrome, caused by a maternally inherited, relatively common A3243G point mutation in the mitochondrial chromosome. Here the hypothesis is examined by a review of Darwin's symptoms, in comparison to MELAS syndrome, and by an examination of related illnesses in his maternal family.
ABOUT GENETICS: Since 1916, GENETICS (http://www.genetics.org/) has covered high quality, original research on a range of topics bearing on inheritance, including population and evolutionary genetics, complex traits, developmental and behavioral genetics, cellular genetics, gene expression, genome integrity and transmission, and genome and systems biology. GENETICS, a peer-reviewed, peer-edited journal of the Genetics Society of America is one of the world's most cited journals in genetics and heredity.
ABOUT GSA: Founded in 1931, the Genetics Society of America (GSA) is the professional membership organization for scientific researchers, educators, bioengineers, bioinformaticians and others interested in the field of genetics. Its nearly 5,000 members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level. GSA is dedicated to promoting research in genetics and to facilitating communication among geneticists worldwide through its conferences, including the biennial conference on Model Organisms to Human Biology, an interdisciplinary meeting on current and cutting edge topics in genetics research, as well as annual and biennial meetings that focus on the genetics of particular organisms, including C. elegans, Drosophila, fungi, mice, yeast, and zebrafish. GSA publishes GENETICS, a leading journal in the field and an online, open-access journal, G3: Genes|Genomes|Genetics. For more information about GSA, please visit www.genetics-gsa.org. Also follow GSA on Facebook at facebook.com/GeneticsGSA and on Twitter @GeneticsGSA.
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