Angiosperms exhibit double fertilization, a process in which one of the sperm cells released from the pollen tube fertilizes the egg, while the other sperm cell fertilizes the central cell, giving rise to the embryo and endosperm, respectively. We have previously reported two polar nuclear fusion-defective double knockout mutants of Arabidopsis thaliana immunoglobulin binding protein (BiP), a molecular chaperone of the heat shock protein 70 (Hsp70) localized in the endoplasmic reticulum (ER), (bip1 bip2) and its partner ER-resident J-proteins, ERdj3A and P58IPK (erdj3a p58ipk). These mutants are defective in the fusion of outer nuclear membrane and exhibit characteristic seed developmental defects after fertilization with wild-type pollen, which are accompanied by aberrant endosperm nuclear proliferation. In this study, we used time-lapse live-cell imaging analysis to determine the cause of aberrant endosperm nuclear division in these mutant seeds. We found that the central cell of bip1 bip2 or erdj3a p58ipk double mutant female gametophytes was also defective in sperm nuclear fusion at fertilization. Sperm nuclear fusion was achieved after the onset of the first endosperm nuclear division. However, division of the condensed sperm nucleus resulted in aberrant endosperm nuclear divisions and delayed expression of paternally derived genes. By contrast, the other double knockout mutant, erdj3b p58ipk, which is defective in the fusion of inner membrane of polar nuclei but does not show aberrant endosperm nuclear proliferation, was not defective in sperm nuclear fusion at fertilization. We thus propose that premitotic sperm nuclear fusion in the central cell is critical for normal endosperm nuclear proliferation.

中文翻译：

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正常的胚乳核增殖需要受精耦合的精子核融合。

被子植物表现出双重受精，在这个过程中，从花粉管释放的一个精子细胞使卵子受精，而另一个精子细胞使中心细胞受精，分别产生胚胎和胚乳。我们以前曾报道过两个拟南芥免疫球蛋白结合蛋白（BiP）的两个极性核融合缺陷双敲除突变体，一种位于内质网（ER）的热休克蛋白70（Hsp70）的分子伴侣，（bip1 bip2）及其ER驻留J蛋白的伴侣，ERdj3A和P58IPK（erdj3a p58ipk）。这些突变体在外核膜融合方面有缺陷，并在与野生型花粉受精后表现出特征性的种子发育缺陷，并伴有异常的胚乳核增殖。在这项研究中，我们使用延时活细胞成像分析来确定这些突变种子中胚乳核分裂异常的原因。我们发现bip1 bip2或erdj3a p58ipk双突变雌配子体的中央细胞在受精时的精子核融合中也有缺陷。第一次胚乳核分裂开始后，实现了精子核融合。但是，精子浓缩核分裂导致异常的胚乳核分裂并延迟了父本衍生基因的表达。相比之下，另一个双敲除突变体erdj3b p58ipk，在极核内膜融合中有缺陷，但没有表现出异常的胚乳核增殖，在受精时没有精子核融合缺陷。