Involvement of Mos-MEK-MAPK pathway in cytostatic factor (CSF) arrest in eggs of the parthenogenetic insect, Athalia rosae

Involvement of Mos-MEK-MAPK pathway in cytostatic factor (CSF) arrest in eggs of the parthenogenetic insect, Athalia rosae
复制标题

DOI:
10.1016/j.mod.2008.08.004
复制
发表时间:
2008-11-01
影响因子:
2.6
通讯作者:
Hatakeyama, Masatsugu
Hatakeyama, Masatsugu
中科院分区:
生物学4区
文献类型:
--
作者:
Yamamoto, Daisuke S.;Tachibana, Kazunori;Hatakeyama, Masatsugu

文献摘要

被引文献

相似文献

对脊椎动物卵母细胞成熟过程中减数分裂中期 II 停滞的广泛调查表明,由 c-mos 原癌基因产物 Mos 调节的丝裂原激活蛋白激酶 (MAPK) 通路在细胞抑制活性(称为细胞抑制因子 (CSF))中具有重要作用。相比之下,对于无脊椎动物中减数分裂停滞在大多数情况下发生在中期 I(MI 停滞)的情况知之甚少。一种孤雌生殖昆虫,锯蝇 Athalia rosae,可以进行人工卵激活,具有研究 MI 阻滞机制的优势。 MAPK/细胞外信号调节蛋白激酶激酶 (MEK) 和 MAPK 在 MI 捕获的锯蝇卵中均被磷酸化并保持活性,而在卵激活后不久它们就去磷酸化。用 MEK 抑制剂 U0126 处理 MI 停滞的卵,导致 MAPK 去磷酸化,MI 停滞得以恢复。克隆并分析了编码丝氨酸/苏氨酸激酶的锯蝇 c-mos 基因直系同源物。它在卵巢的护理细胞中表达。为了检查锯蝇 Mos 的 CSF 活性,将合成的谷胱甘肽 S-转移酶 (GST) 融合锯蝇 Mos 蛋白注射到 MEK 和 MAPK 去磷酸化的 MI 恢复卵中。 MEK 和 MAPK 均在注射后再次磷酸化。在这些 GST 融合锯蝇注射 Mos 的卵中,随后的有丝分裂(合胞体)分裂被阻断,胚胎发育停止。这些结果表明,MEK-MAPK 通路参与维持锯蝇卵中 CSF 的停滞,并且 Mos 充当其上游调节分子。 (c) 2008 Elsevier Ireland Ltd. 保留所有权利。
Extensive survey of meiotic metaphase II arrest during oocyte maturation in vertebrates revealed that the mitogen-activated protein kinase ( MAPK) pathway regulated by the c-mos proto-oncogene product, Mos, has an essential role in cytostatic activity, termed cytostatic factor (CSF). In contrast, little is known in invertebrates in which meiotic arrest occurs in most cases at metaphase I (MI arrest). A parthenogenetic insect, the sawfly Athalia rosae, in which artificial egg activation is practicable, has advantages to investigate the mechanisms of MI arrest. Both the MAPK/extracellular signal-regulated protein kinase kinase (MEK) and MAPK were phosphorylated and maintained active in MI-arrested sawfly eggs, whereas they were dephosphorylated soon after egg activation. Treatment of MI-arrested eggs with U0126, an inhibitor of MEK, resulted in dephosphorylation of MAPK and MI arrest was resumed. The sawfly c-mos gene orthologue encoding a serine/threonine kinase was cloned and analyzed. It was expressed in nurse cells in the ovaries. To examine CSF activity of the sawfly Mos, synthesized glutathione S-transferase (GST)fusion sawfly Mos protein was injected into MI-resumed eggs in which MEK and MAPK were dephosphorylated. Both MEK and MAPK were phosphorylated again upon injection. In these GST-fusion sawfly Mos-injected eggs subsequent mitotic ( syncytial) divisions were blocked and embryonic development was ceased. These results demonstrated that the MEK-MAPK pathway was involved in maintaining CSF arrest in sawfly eggs and Mos functioned as its upstream regulatory molecule. (c) 2008 Elsevier Ireland Ltd. All rights reserved.