线虫(Caenorhabditis elegans)多年来一直是一个遗传模型体系,但这篇论文是第一篇识别出这些生物一个经典多态性背后的一个基因的论文。一些种类的雄性在交配后能在雌性体内留下一个粘性塞子,而其他种类的雄性却不能。Palopoli等人发现,这是由于为一种像粘蛋白一样的蛋白编码的一个基因所发生的变化,这个变化能够在全世界的线虫种群中传播开来。
原始出处:
Nature 454, 1019-1022 (21 August 2008) | doi:10.1038/nature07171
Molecular basis of the copulatory plug polymorphism in Caenorhabditis elegans
Michael F. Palopoli1,3, Matthew V. Rockman2,3, Aye TinMaung1, Camden Ramsay1, Stephen Curwen1, Andrea Aduna1, Jason Laurita1 & Leonid Kruglyak2
Department of Biology, Bowdoin College, 6500 College Station, Brunswick, Maine 04011, USA
Lewis-Sigler Institute for Integrative Genomics and Department of Ecology and Evolutionary Biology, Carl Icahn Laboratory, Princeton University, Princeton, New Jersey 08544, USA
These authors contributed equally to this work.
Heritable variation is the raw material for evolutionary change, and understanding its genetic basis is one of the central problems in modern biology. We investigated the genetic basis of a classic phenotypic dimorphism in the nematode Caenorhabditis elegans. Males from many natural isolates deposit a copulatory plug after mating, whereas males from other natural isolates?including the standard wild-type strain (N2 Bristol) that is used in most research laboratories?do not deposit plugs1. The copulatory plug is a gelatinous mass that covers the hermaphrodite vulva, and its deposition decreases the mating success of subsequent males2. We show that the plugging polymorphism results from the insertion of a retrotransposon into an exon of a novel mucin-like gene, plg-1, whose product is a major structural component of the copulatory plug. The gene is expressed in a subset of secretory cells of the male somatic gonad, and its loss has no evident effects beyond the loss of male mate-guarding. Although C. elegans descends from an obligate-outcrossing, male?female ancestor3, 4, it occurs primarily as self-fertilizing hermaphrodites5, 6, 7. The reduced selection on male?male competition associated with the origin of hermaphroditism may have permitted the global spread of a loss-of-function mutation with restricted pleiotropy.