cDNA cloning, expression, subcellular localization, and chromosomal assignment of mammalian aurora homologues, aurora-related kinase (ARK) 1 and 2
cDNA cloning, expression, subcellular localization, and chromosomal assignment of mammalian aurora homologues, aurora-related kinase (ARK) 1 and 2
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DOI：
10.1006/bbrc.1998.8250
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发表时间：
1998-03-06
影响因子：
3.1
通讯作者：
Okumura, K
中科院分区：
文献类型：
--
作者：
Shindo, M;Nakano, H;Okumura, K
有丝分裂和减数分裂过程中的染色体分离被认为是由多种激酶调节的，但确切的机制仍然很大程度上未知。果蝇中的一个突变（称为极光）被确定为染色体分离缺陷的负责基因，并编码假定的丝氨酸-苏氨酸激酶。在这里，我们鉴定了哺乳动物极光同源物，命名为极光相关激酶 (ARK) 1 和 ARK2。鼠 ARK1 和 ARK2 的激酶结构域在氨基酸水平上分别与 aurora 的激酶结构域有 61% 和 62% 的同一性。细胞周期分析显示ARK1的表达与G2/M期相关，而ARK2在S期和G2/M期表达。免疫荧光分析表明，ARK2 主要定位于中体，而 ARK1 据报道在有丝分裂期间定位于纺锤体极。总的来说，这些结果表明这两种激酶在细胞周期进程中可能具有不同的表达时间和亚细胞定位的不同作用。种间回交作图显示，Ark1 位于小鼠 2 号染色体的远端区域，而 Ark2 位于小鼠 11 号染色体的中央区域。(C) 1998 年学术出版社。
Chromosomal segregation during mitosis as well as meiosis is considered to be regulated by multiple kinases, but the precise mechanism remains largely unknown. A mutation in Drosophila, designated aurora, was identified as a responsible gene for a chromosomal segregation defect and encodes a putative serine-threonine kinase. Here we have identified mammalian aurora homologues, designated aurora-related kinase (ARK) 1 and ARK2. Kinase domains of murine ARK1 and ARK2 showed 61 and 62% identity, respectively, to that of aurora at the amino acid levels, respectively. Cell cycle analysis revealed that the expression of ARK1 was correlated with G2/M phase, while ARK2 was expressed during S and G2/M phases. Immunofluorescence analysis demonstrated that ARK2 was mainly localized to the midbody, while ARK1 has been reported to be localized to the spindle pole during mitosis. Collectively, these results suggest that these two kinases may have distinct roles with different expression timing and subcellular localization during the cell cycle progression. Interspecific backcross mapping revealed that Ark1 is located in a distal region of mouse chromosome 2, while Ark2 is located in a central region of mouse chromosome 11. (C) 1998 Academic Press.