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RNA病毒ϕ6单个基因中有害和有益突变的显性效应

Dominance effects of deleterious and beneficial mutations in a single gene of the RNA virus ϕ6.

作者信息

Joseph Sarah B, Peck Kayla M, Burch Christina L

机构信息

Department of Biology, University of North Carolina, Chapel Hill, North Carolina, United States of America.

出版信息

PLoS One. 2014 Jun 19;9(6):e97717. doi: 10.1371/journal.pone.0097717. eCollection 2014.

DOI:10.1371/journal.pone.0097717
PMID:24945910
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4063744/
Abstract

Most of our knowledge of dominance stems from studies of deleterious mutations. From these studies we know that most deleterious mutations are recessive, and that this recessivity arises from a hyperbolic relationship between protein function (i.e., protein concentration or activity) and fitness. Here we investigate whether this knowledge can be used to make predictions about the dominance of beneficial and deleterious mutations in a single gene. We employed a model system--the bacteriophage φ6--that allowed us to generate a collection of mutations in haploid conditions so that it was not biased toward either dominant beneficial or recessive deleterious mutations. Screening for the ability to infect a bacterial host that does not permit infection by the wildtype φ6, we generated a collection of mutations in P3, a gene involved in attachment to the host and in phage particle assembly. The resulting collection contained mutations with both deleterious and beneficial effects on fitness. The deleterious mutations in our collection had additive effects on fitness and the beneficial mutations were recessive. Neither of these observations were predicted from previous studies of dominance. This pattern is not consistent with the hyperbolic (diminishing returns) relationship between protein function and fitness that is characteristic of enzymatic genes, but could have resulted from a curve of increasing returns.

摘要

我们对显性的大部分认识源于对有害突变的研究。从这些研究中我们知道,大多数有害突变是隐性的,并且这种隐性源于蛋白质功能(即蛋白质浓度或活性)与适应性之间的双曲线关系。在这里,我们研究这些知识是否可用于预测单个基因中有益和有害突变的显性情况。我们采用了一个模型系统——噬菌体φ6——它使我们能够在单倍体条件下产生一系列突变,从而不会偏向于显性有益突变或隐性有害突变。通过筛选感染野生型φ6无法感染的细菌宿主的能力,我们在P3基因中产生了一系列突变,P3基因参与宿主附着和噬菌体颗粒组装。产生的一系列突变包含对适应性有有害和有益影响的突变。我们所研究的有害突变对适应性具有累加效应,而有益突变是隐性的。这两个观察结果都不是先前对显性的研究所预测到的。这种模式与酶基因特有的蛋白质功能与适应性之间的双曲线(收益递减)关系不一致,但可能是由收益递增曲线导致的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/aeb174503c52/pone.0097717.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/79400b5650fd/pone.0097717.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/9c7f1f432563/pone.0097717.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/4d4ce18ffe4a/pone.0097717.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/ca9306c1c322/pone.0097717.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/d846cbf5fa37/pone.0097717.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/aeb174503c52/pone.0097717.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/79400b5650fd/pone.0097717.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/9c7f1f432563/pone.0097717.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/4d4ce18ffe4a/pone.0097717.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/ca9306c1c322/pone.0097717.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/d846cbf5fa37/pone.0097717.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef93/4063744/aeb174503c52/pone.0097717.g006.jpg

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