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缺失对丽蝇蛹集金小蜂父本性别比(PSR)染色体有丝分裂稳定性的影响。

Effects of deletions on mitotic stability of the paternal-sex-ratio (PSR) chromosome from Nasonia.

作者信息

Beukeboom L W, Reed K M, Werren J H

机构信息

Department of Biology, University of Rochester, NY 14627.

出版信息

Chromosoma. 1992 Dec;102(1):20-6. doi: 10.1007/BF00352286.

Abstract

Paternal-Sex-Ratio (PSR) is a B chromosome that causes all-male offspring in the parasitoid wasp Nasonia vitripennis. It is only transmitted via sperm of carrier males and destroys the other paternal chromosomes during the first mitotic division of the fertilized egg. Because of haplodiploidy, the effect of PSR is to convert diploid (female) eggs into haploid eggs that develop into PSR-bearing males. The PSR chromosome was previously found to contain several families of repetitive DNA, which appear to be present in local blocks. PSR chromosomes with irradiation-induced deletions have decreased rates of transmission and increased variation in transmission. This study investigates whether these differences in transmission of deletion chromosomes are due to mitotic instability. Two deletion chromosomes (E306 and F316) and the wild-type PSR chromosome were examined. A cytogenetic assay of testes revealed that wild-type PSR males contained the chromosome in 98%-100% of their spermatocytes. Similar counts from carriers of two deletion chromosomes were lower and varied between individuals from 50%-100%. One F316 male did not contain the chromosome in any of its spermatocytes although the chromosome was present in somatic tissues based on hybridization to PSR-specific repetitive DNA. A molecular analysis of males found the wild-type PSR chromosome to be present in all somatic tissues. Tissue specific differences in the presence of PSR were found in several males from the two deletion lines. The results show that deletions can result in mosaicism due to increased mitotic instability of PSR. Such individuals sometimes partially or completely fail to transmit the chromosome.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

父本性别比(PSR)是一种B染色体,它会导致寄生蜂丽蝇蛹集金小蜂产生全雄后代。它仅通过携带该染色体的雄性的精子进行传播,并在受精卵的第一次有丝分裂过程中破坏其他父本染色体。由于单双倍体现象,PSR的作用是将二倍体(雌性)卵转化为单倍体卵,这些单倍体卵发育成携带PSR的雄性。先前发现PSR染色体包含几个重复DNA家族,它们似乎以局部区域的形式存在。具有辐射诱导缺失的PSR染色体的传递率降低,传递变异增加。本研究调查了缺失染色体传递的这些差异是否是由于有丝分裂不稳定性所致。研究检测了两条缺失染色体(E306和F316)以及野生型PSR染色体。对睾丸的细胞遗传学分析表明,野生型PSR雄性的精母细胞中有98%-100%含有该染色体。两条缺失染色体携带者的类似计数较低,个体之间在50%-100%之间变化。一只F316雄性的任何精母细胞中都不含有该染色体,尽管基于与PSR特异性重复DNA的杂交,该染色体存在于体细胞组织中。对雄性的分子分析发现野生型PSR染色体存在于所有体细胞组织中。在来自两个缺失系的几只雄性中发现了PSR存在的组织特异性差异。结果表明,由于PSR有丝分裂不稳定性增加,缺失可导致嵌合体现象。这样的个体有时会部分或完全无法传递该染色体。(摘要截短至250字)

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