The Acp26Aa seminal fluid protein is a modulator of early egg hatchability in Drosophila melanogaster
The Acp26Aa seminal fluid protein is a modulator of early egg hatchability in Drosophila melanogaster
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DOI：
10.1098/rspb.2001.1684
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发表时间：
2001-08-22
影响因子：
4.7
通讯作者：
Wolfner, MF
中科院分区：
文献类型：
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作者：
Chapman, T;Herndon, LA;Wolfner, MF
黑腹果蝇（Drosophila melanogaster）的雄性附属腺蛋白（male accessory gland proteins, Acps）在精液中随精子一起转移，介导雄性之间交配后的受精竞争。Acps的作用包括对排卵、接受性和精子储存的影响。调节卵子产生的两个Acps是Acp26Aa（排卵素）和Acp70A（性肽）。Acp26Aa特异性作用于排卵过程（在交配后1.5小时开始从卵巢释放成熟卵子）。相比之下，精子的储存可能需要长达6-9英里的时间才能完成。因此，处女交配后的初始排卵将发生在所有精子完全储存之前，并且由于Acp26Aa转移而最初产下的额外卵子预计将无法有效受精。acp26aa介导的现有卵子的释放不应该造成显著的能量消耗或导致雌性寿命的减少，假设产卵的能量消耗来自于卵子的新生合成（卵发生）而不是排卵。我们用Acp26Aa(1)突变雄性来测试这些预测，这些突变雄性缺乏Acp26Aa，但对其他Acps和Acp26Aa(2)突变雄性来说是正常的，它们转移了一个截断但功能完整的Acp26Aa蛋白。与Acp26Aa(2)截断的雄性交配的雌性在第一次交配后产生的卵子明显多于Acp26Aa(1)（零）的雄性。然而，正如上文所预测的那样，这些由于Acp26Aa转移到处女雌性而产下的额外卵，显示出显著降低的卵孵化率。对照试验表明，这种较低的孵化率是由于交配后早期的受精率较低。在随后的非处女交配中，卵的孵化率没有下降。此外，如上所述，接受或未接受Acp26Aa的雌性在存活率、终身繁殖力和终身后代方面没有差异，这表明Acp26Aa的转移并不代表雌性的显著能量成本，也不会增加交配的生存成本。Acp26Aa似乎通过清除现有的成熟卵子，从而间接地允许在交配后立即开始卵子发生，从而消除了卵子发生的障碍。结果表明，在交配对中，微妙的过程协调了卵子产生和精子储存的刺激。
Drosophila melanogaster male accessory gland proteins (Acps) that are transferred in the ejaculate with sperm mediate post-mating competition for fertilizations between males. The actions of Acps include effects on oviposition and ovulation, receptivity and sperm storage. Two Acps that modulate egg production are Acp26Aa (ovulin) and Acp70A (the sex peptide). Acp26Aa acts specifically on the process of ovulation (the release of mature eggs from the ovaries which is initiated 1.5 h after mating. In contrast, sperm storage can take as long as 6-9 li to complete. Initial ovulations after matings by virgin females will therefore occur before all sperm are fully stored and the extra eggs initially laid as a result of Acp26Aa transfer are expected to be inefficiently fertilized. Acp26Aa-mediated release of existing eggs should not cause a significant energetic cost or lead to a decrease in female lifespan assuming, as seems likely, that the energetic cost of egg laying comes from de novo egg synthesis (oogenesis') rather than from ovulation. We tested these predictions using Acp26Aa(1) mutant males that lack Acp26Aa but are normal for other Acps and Acp26Aa(2) males that transfer a truncated but fully functional Acp26Aa protein. Females mating with Acb26Aa(2) truncation) males that received functional Acp26Aa produced significantly more eggs following their first matings than did mates of Acp26Aa(1) (null) males. However, as predicted above, these extra eggs, which were laid as a result of Acp26Aa transfer to virgin females, showed significantly lower egg hatchability. Control experiments indicated that this lower hatchability was due to lower rates of fertilization at early post-mating times. There was no drop in egg hatchability in subsequent nonvirgin matings. In addition, as predicted above, females that did or did not receive Acp26Aa did not differ in survival, lifetime fecundity or lifetime progeny, indicating that Acp26Aa transfer does not represent a significant energetic cost ibr females and does not contribute to the survival cost of mating. Acp26Aa appears to remove a block to oogenesis by causing the clearing out of existing mature eggs and, thus, indirectly allowing oogenesis to be initiated immediately after mating. The results show that subtle processes coordinate the stimulation of egg production and sperm storage in mating pairs.