The role of MATER in endoplasmic reticulum distribution and calcium homeostasis in mouse oocytes.
The role of MATER in endoplasmic reticulum distribution and calcium homeostasis in mouse oocytes.
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DOI：
10.1016/j.ydbio.2013.12.025
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发表时间：
2014-02-15
影响因子：
2.7
通讯作者：
Coonrod, Scott A.
中科院分区：
文献类型：
--
作者：
Kim, Boram;Zhang, Xuesen;Kan, Rui;Cohen, Roy;Mukai, Chinatsu;Travis, Alexander J.;Coonrod, Scott A.
Ca2+振荡是哺乳动物受精的标志，在发育激活中发挥核心作用。这些振荡所需的钙主要来自内质网 (ER)，内质网在卵母细胞成熟过程中聚集在微绒毛皮层下。成熟过程中 ER 向皮质的迁移被认为在使 ER 有能力产生钙瞬变方面发挥着重要作用，并且 ER 的重新分布被认为主要由微管和微丝介导。我们之前已经表明，卵母细胞和早期胚胎限制性母体效应基因 Mater (Nlrp5) 定位于卵母细胞胞质格子的形成，并且是卵母细胞胞质格子形成所必需的，卵母细胞胞质格子是一种含有微管蛋白的结构，似乎在卵母细胞成熟过程中细胞器的定位和分布中发挥着重要作用。鉴于这些观察结果，我们假设卵母细胞中 ER 重新分配和 Ca2+ 稳态也可能需要 Mater。为了检验这一假设，我们首先研究了中期 II Matertm/tm（亚形）卵母细胞中的 ER 定位，发现与野生型卵母细胞相比，微绒毛皮质处的 ER 簇较少丰富。为了研究 MATER 介导 ER 重新分布的潜在机制，我们测试了突变卵母细胞中微管蛋白表达水平和定位是否受到影响，并发现 Matertm/tm 卵母细胞中微管蛋白的 Triton 不溶部分显着减少。为了确定与这些 ER 异常相关的潜在功能缺陷，我们接下来着手研究体外受精后 Matertm/tm 卵母细胞中 Ca2+ 振荡的模式是否发生改变。有趣的是，与野生型卵母细胞相比，Matertm/tm 卵母细胞中的 Ca2+ 振荡表现出显着较低的第一峰值振幅和较高的频率。然后我们发现 Matertm/tm 卵母细胞中的 Ca2+ 振荡缺陷可能是由于 ER 储存中 Ca2+ 量减少引起的。总而言之，这些观察结果支持这样的假设：MATER 是卵母细胞中 ER 分布和 Ca2+ 稳态所必需的，这可能是由于晶格介导的 ER 定位和/或重新分布的缺陷所致。
Ca2+ oscillations are a hallmark of mammalian fertilization and play a central role in the activation of development. The calcium required for these oscillations is primarily derived from the endoplasmic reticulum (ER), which accumulates in clusters at the microvillar subcortex during oocyte maturation. The migration of the ER to the cortex during maturation is thought to play an important role in rendering the ER competent to generate the calcium transients, and the redistribution of ER is believed to be primarily mediated by microtubules and microfilaments. We have previously shown that the oocyte- and early embryo-restricted maternal effect gene Mater (Nlrp5) localizes to, and is required for, formation of the oocyte cytoplasmic lattices, a tubulin-containing structure that appears to play an important role in organelle positioning and distribution during oocyte maturation. Given these observations, we hypothesized that Mater may also be required for ER redistribution and Ca2+ homeostasis in oocytes. To test this hypothesis, we first investigated ER localization in metaphase-II Matertm/tm (hypomorph) oocytes and found ER clusters to be less abundant at the microvillar cortex when compared to wild type oocytes. To examine the potential mechanisms by which MATER mediates ER redistribution, we tested whether tubulin expression levels and localization were affected in the mutant oocytes and found that the Triton-insoluble fraction of tubulin was significantly decreased in Matertm/tm oocytes. To identify potential functional defects associated with these ER abnormalities, we next set out to investigate if the pattern of Ca2+ oscillations was altered in Matertm/tm oocytes after fertilization in vitro. Intriguingly, Ca2+ oscillations in Matertm/tm oocytes exhibited a significantly lower first peak amplitude and a higher frequency when compared to wild type oocytes. We then found that the Ca2+ oscillation defect in Matertm/tm oocytes was likely caused by a reduced amount of Ca2+ in the ER stores. Taken together, these observations support the hypothesis that MATER is required for ER distribution and Ca2+ homeostasis in oocytes, likely due to defects in lattice-mediated ER positioning and/or redistribution.
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影响因子：
3.7
作者：
Kim B;Kan R;Anguish L;Nelson LM;Coonrod SA
通讯作者：
Coonrod SA
影响因子：
3.6
作者：
MEHLMANN, LM;KLINE, D
通讯作者：
KLINE, D
影响因子：
2.7
作者：
Kline, D;Mehlmann, L;Terasaki, M
通讯作者：
Terasaki, M
影响因子：
2.7
作者：
Mehlmann, LM;Mikoshiba, K;Kline, D
通讯作者：
Kline, D
影响因子：
56.9
作者：
MIYAZAKI, S;YUZAKI, M;MIKOSHIBA, K
通讯作者：
MIKOSHIBA, K