Echinoderm Microtubule Associated Protein Like 1 Is Indispensable for Oocyte Spindle Assembly and Meiotic Progression in Mice.
Echinoderm Microtubule Associated Protein Like 1 Is Indispensable for Oocyte Spindle Assembly and Meiotic Progression in Mice.
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棘皮动物微管相关蛋白样 1 对于小鼠卵母细胞纺锤体组装和减数分裂进程不可或缺
DOI：
10.3389/fcell.2021.687522
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发表时间：
2021
影响因子：
5.5
通讯作者：
Su YQ
中科院分区：
文献类型：
--
作者：
Yin H;Zhang T;Wang H;Hu X;Hou X;Fang X;Yin Y;Li H;Shi L;Su YQ
Completion of the first meiosis is an essential prerequisite for producing a functionally normal egg for fertilization and embryogenesis, but the precise mechanisms governing oocyte meiotic progression remains largely unclear. Here, we report that echinoderm microtubule associated protein (EMAP) like 1 (EML1), a member of the conserved EMAP family proteins, plays a crucial role in the control of oocyte meiotic progression in the mouse. Female mice carrying an ENU-induced nonsense mutation (c.1956T > A; p.Tyr652∗) of Eml1 are infertile, and the majority of their ovulated oocytes contain abnormal spindles and misaligned chromosomes. In accordance with the mutant oocyte phenotype, we find that EML1 is colocalized with spindle microtubules during the process of normal oocyte meiotic maturation, and knockdown (KD) of EML1 by specific morpholinos in the fully grown oocytes (FGOs) disrupts the integrity of旋转和减数分裂的进展。 Otubulles和中期I处的主轴组件检查点的正确失活（MI）。EML1的损失还会损害卵母细胞恢复和完成第一个减数分裂的促进因素的激活，当通过WEE1/2抑制剂PD166285纠正时，它可以有效地响应型卵形延迟的效率。基因C（NUDC），体细胞中的关键有丝分裂调节剂细胞，EML1-KD破坏了NUDC在卵母细胞纺锤体上的特异性定位，这些数据表明EML1调节了囊体纺锤体的形成以及在哺乳动物卵母细胞中减数分裂向MII的进展，这可能是由不同的机制介导的。
Completion of the first meiosis is an essential prerequisite for producing a functionally normal egg for fertilization and embryogenesis, but the precise mechanisms governing oocyte meiotic progression remains largely unclear. Here, we report that echinoderm microtubule associated protein (EMAP) like 1 (EML1), a member of the conserved EMAP family proteins, plays a crucial role in the control of oocyte meiotic progression in the mouse. Female mice carrying an ENU-induced nonsense mutation (c.1956T > A; p.Tyr652∗) of Eml1 are infertile, and the majority of their ovulated oocytes contain abnormal spindles and misaligned chromosomes. In accordance with the mutant oocyte phenotype, we find that EML1 is colocalized with spindle microtubules during the process of normal oocyte meiotic maturation, and knockdown (KD) of EML1 by specific morpholinos in the fully grown oocytes (FGOs) disrupts the integrity of spindles, and delays meiotic progression. Moreover, EML1-KD oocytes fail to progress to metaphase II (MII) stage after extrusion of the first polar body, but enter into interphase and form a pronucleus containing decondensed chromatins. Further analysis shows that EML1-KD impairs the recruitment of γ-tubulin and pericentrin to the spindle poles, as well as the attachment of kinetochores to microtubules and the proper inactivation of spindle assembly checkpoint at metaphase I (MI). The loss of EML1 also compromises the activation of maturation promoting factor around the time of oocyte resumption and completion of the first meiosis, which, when corrected by WEE1/2 inhibitor PD166285, efficiently rescues the phenotype of oocyte delay of meiotic resumption and inability of reaching MII. Through IP- mass spectrometry analysis, we identified that EML1 interacts with nuclear distribution gene C (NUDC), a critical mitotic regulator in somatic cells, and EML1-KD disrupts the specific localization of NUDC at oocyte spindles. Taken together, these data suggest that EML1 regulates acentrosomal spindle formation and the progression of meiosis to MII in mammalian oocytes, which is likely mediated by distinct mechanisms.
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影响因子：
4.5
作者：
Colombié N;Głuszek AA;Meireles AM;Ohkura H
通讯作者：
Ohkura H
影响因子：
3.7
作者：
Brunet S;Dumont J;Lee KW;Kinoshita K;Hikal P;Gruss OJ;Maro B;Verlhac MH
通讯作者：
Verlhac MH
影响因子：
4.6
作者：
Collin, G. B.;Won, J.;Nishina, P. M.
通讯作者：
Nishina, P. M.
MTOR 卵母细胞阶段特异性影响决定小鼠颗粒细胞命运和卵母细胞质量
DOI：
10.1073/pnas.1800352115
发表时间：
2018-06-05
影响因子：
11.1
作者：
Guo J;Zhang T;Guo Y;Sun T;Li H;Zhang X;Yin H;Cao G;Yin Y;Wang H;Shi L;Guo X;Sha J;Eppig JJ;Su YQ
通讯作者：
Su YQ
影响因子：
64.8
作者：
COLLEDGE, WH;CARLTON, MBL;EVANS, MJ
通讯作者：
EVANS, MJ