The Drosophila misfire gene has an essential role in sperm activation during fertilization
The Drosophila misfire gene has an essential role in sperm activation during fertilization
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DOI：
10.1266/ggs.78.253
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发表时间：
2003-06-01
影响因子：
1.1
通讯作者：
Yamamoto, MT
中科院分区：
文献类型：
--
作者：
Ohsako, T;Hirai, K;Yamamoto, MT
果蝇雄性不育突变misfire（mfr）是一种新的父本效应受精缺陷突变体，它影响精子头部解凝聚。MFR精子是能动的，形态正常，并在交配期间转移到雌性体内。然而，不到0.1%的产卵的女性交配的mfr男性孵化。尽管mfr精子进入卵子的频率很高（93%），但99%的受精卵子并未启动第一次核分裂。与野生型精子不同，精子尾部在卵内的位置和形状并不恒定，而是以看似随机的方式变化。受精突变体精子的头部总是位于卵表面附近，正好位于卵质膜之下，并保持其针状形状，表明核解凝聚失败。进一步观察发现，受精精子的质膜似乎是完整的，包括头部区域。这些表型与另一种受精缺陷型雄性不育突变体sneaky（snky）的表型相当。我们的观察结果强烈表明，mfr突变的雄性不育，因为他们的受精精子不能形成雄性原核，这是由于精子不能对负责质膜破裂的卵因子做出适当的反应。虽然mfr和snky突变在表型上是相同的，但它们定位于细胞学上不同的遗传位点，没有观察到遗传相互作用，这表明至少有两种不同的父系基因产物参与了原核形成的早期阶段。
The male sterile mutation, misfire (mfr), of Drosophila melanogaster is a novel paternal effect, fertilization defective mutant that effects sperm head decondensation. mfr sperm were motile, appeared normal morphologically and were transferred to the female during copulation. However, less than 0.1% of eggs laid by females mated to mfr males hatched. Although mfr sperm entered eggs at a high frequency (93%), 99% of the inseminated eggs did not initiate the first nuclear division. Unlike wild type fertilizing sperm, the position and shape of mfr sperm tails within the egg were not constant, but varied in a seemingly random manner. The heads of inseminating mutant sperm were always located near the surface of eggs just underlying the egg plasma membrane, and maintained their needle-like shape indicating the failure of nuclear decondensation. Further observations revealed that plasma membrane of inseminating sperm appeared intact, including the head region. These phenotypes were equivalent to those of sneaky (snky), another fertilization defective male sterile mutation. Our observations strongly suggest that mfr mutant males are sterile because their inseminating sperm fail to form a male pronucleus due to the inability of the sperm to properly respond to egg factors responsible for the breakdown of the plasma membrane. Although mfr and snky mutations were phenotypically identical, they mapped to cytologically distinct genetic loci and no genetic interactions were observed, suggesting that at least two distinct paternal gene products are involved in the early stages of pronuclear formation.