線蟲（Caenorhabditis elegans）多年來一直是一個遺傳模型體系,，但這篇論文是第一篇識別出這些生物一個經典多態(tài)性背后的一個基因的論文,。一些種類的雄性在交配后能在雌性體內留下一個粘性塞子，而其他種類的雄性卻不能,。Palopoli等人發(fā)現(xiàn),，這是由于為一種像粘蛋白一樣的蛋白編碼的一個基因所發(fā)生的變化，這個變化能夠在全世界的線蟲種群中傳播開來,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
