An extra copy of nimEcyclinB elevates pre-MPF levels and partially suppresses mutation of nimTcdc25 in Aspergillus nidulans.

An extra copy of nimEcyclinB elevates pre-MPF levels and partially suppresses mutation of nimTcdc25 in Aspergillus nidulans.
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nimEcyclinB 的额外拷贝可提高构巢曲霉中 MPF 前的水平并部分抑制 nimTcdc25 的突变。

DOI:
10.1002/j.1460-2075.1992.tb05273.x
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发表时间:
1992
期刊:
The EMBO journal
影响因子:
--
通讯作者:
Osmani,SA
Osmani,SA
中科院分区:
--
文献类型:
--
作者:
O'Connell,MJ;Osmani,AH;Morris,NR;Osmani,SA

文献摘要

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先前的工作表明,NIMA编码一种细胞周期调节的蛋白激酶,它与p34cdc2组蛋白H1激酶(MPF)一起是有丝分裂所必需的。我们现在已经确定了另外两种在有丝分裂中所需的基因产物。NIMT编码一种类似于分裂酵母CDC25酪氨酸磷酸酶的蛋白质,是将前MPF转化为MPF所必需的,NIME编码一种B型细胞周期蛋白,它是MPF的一个亚单位。报道了nimEcyClinB和nimTcdc25型基因之间的一种新的遗传互作。增加nimEcyClinB的拷贝数可以抑制nimTcdc25的突变,并导致酪氨酸磷酸化p34cdc2(前MPF)的积累增加。这种生化观察为基因互补提供了一种解释。如果nimEcyClinB招募p34cdc2进行酪氨酸磷酸化以形成前MPF,那么nimEcyClinB的表达增加将增加前MPF的水平。产生的前MPF水平的增加可能会允许突变的nimTcdc25蛋白将足够的前MPF转化为MPF,从而允许一些有丝分裂进程。我们还证明了p34cdc2蛋白激酶通路的正确细胞周期调节对于空肠弯曲菌正确的发育进程是必不可少的。
Previous work has shown that nimA encodes a cell cycle regulated protein kinase that is required along with the p34cdc2 histone H1 kinase (MPF) for mitosis in Aspergillus nidulans. We have now identified two other gene products required for mitosis in A.nidulans. nimT encodes a protein similar to the fission yeast cdc25 tyrosine phosphatase and is required for the conversion of pre‐MPF to MPF and nimE encodes a B‐type cyclin which is a subunit of MPF. A new genetic interaction between nimEcyclinB and nimTcdc25 type genes is reported. Increased copy number of nimEcyclinB can suppress mutation of nimTcdc25 and also lead to increased accumulation of tyrosine phosphorylated p34cdc2 (pre‐MPF). This biochemical observation suggests an explanation for the genetic complementation. If nimEcyclinB recruits p34cdc2 for tyrosine phosphorylation to form pre‐MPF it follows that increased expression of nimEcyclinB would increase the level of pre‐MPF. The increased level of pre‐MPF generated may then allow the mutant nimTcdc25 protein to convert enough pre‐MPF to MPF and thus permit some mitotic progression. We also demonstrate that correct cell cycle regulation by the p34cdc2 protein kinase pathway is essential for correct developmental progression in A.nidulans.