A genetic test of the role of the maternal pronucleus in Wolbachia-induced cytoplasmic incompatibility in Drosophila melanogaster

A genetic test of the role of the maternal pronucleus in Wolbachia-induced cytoplasmic incompatibility in Drosophila melanogaster
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DOI:
10.1534/genetics.105.053272
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发表时间:
2006-06-01
期刊:
影响因子:
3.3
通讯作者:
Sullivan, William
Sullivan, William
中科院分区:
生物学2区
文献类型:
--
作者:
Ferree, Patrick M.;Sullivan, William

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细胞质不相容性(CI)是节肢动物中发现的一种生殖不育症,由内寄生细菌沃尔巴克氏体引起。在 CI 中,如果感染沃尔巴克氏体的雄性与未感染的雌性受精,宿主后代将无法在早期胚胎发生过程中发育。人们普遍认为,这种致死性是由沃尔巴克氏体引起的宿主睾丸中父本核物质的某些未知修饰引起的。然而,这种修饰导致早期胚胎死亡的直接方式目前尚未解决。先前的研究结果表明,CI 致死性是由于父本和母本原核之间的细胞周期时间不同步而发生的。这一假设可以通过预测沃尔巴克氏体修饰的父本核应支持雄激素发育(即仅来自父本原核)来进行实验检验。利用果蝇中产生雄激素后代的特定突变,我们证明沃尔巴克氏体诱导的修饰抑制了这种类型的发育。这一结果表明 CI 独立于母体原核发生,并反对原核异步作为 CI 致死的主要原因。我们认为 CI 的发生是由于父本原核发育不全或父本原核与卵细胞质细胞周期不同步的结果。
Cytoplasmic incompatibility (CI) is a reproductive sterility found in arthropods that is caused by the endoparasitic bacteria Wolbachia. In CI, host progeny fail to develop during early embryogenesis if Wolbachia-infected males fertilize uninfected females. It is widely accepted that this lethality is caused by some unknown Wolbachia-induced modification of the paternal nuclear material in the host testes. However, the direct means by which this modification leads to early embryonic death are currently unresolved. Results from previous studies suggested that CI lethality occurs as a result of asynchromy in cell cycle timing between the paternal and maternal pronuclei. This hypothesis can be tested experimentally by the prediction that the Wolbachia-modified paternal pronucleus should support androgenetic development (i.e., from the paternal pronucleus only). Using specific mutations in Drosophila melanogaster that produce androgenetic progeny, we demonstrate that the Wolbachia-induced modification inhibits this type of development. This result suggests that CI occurs independently of the maternal pronucleus and argues against pronuclear asynchrony as the primary cause of CI lethality. We propose that CI occurs instead as the result of either a developmentally incompetent paternal pronucleus or asynchrony between the paternal pronucleus and the cell cycle of the egg cytoplasm.