ArticleThe EMBO journal1997
The G2/M DNA damage checkpoint inhibits mitosis through Tyr15 phosphorylation of p34cdc2 in Aspergillus nidulans.
Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 70 citations in OpenAlex.
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- Phylogeny, identification and nomenclature of the genus Aspergillus.Studies in mycology · 2014Article
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- Analysis of all protein phosphatase genes in Aspergillus nidulans identifies a new mitotic regulator, fcp1.Eukaryotic cell · 2009Article
- Genetic interactions of the Aspergillus nidulans atmAATM homolog with different components of the DNA damage response pathway.Genetics · 2008Article
- A point mutation in the Aspergillus nidulans sonBNup98 nuclear pore complex gene causes conditional DNA damage sensitivity.Genetics · 2006Article
- The csnD/csnE signalosome genes are involved in the Aspergillus nidulans DNA damage response.Genetics · 2005Article
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- The Aspergillus nidulans npkA gene encodes a Cdc2-related kinase that genetically interacts with the UvsBATR kinase.Genetics · 2004Article
- The Aspergillus nidulans snt genes are required for the regulation of septum formation and cell cycle checkpoints.Genetics · 2001Article
- A Pcl-like cyclin of Aspergillus nidulans is transcriptionally activated by developmental regulators and is involved in sporulation.Molecular and cellular biology · 2001Article
- Extragenic suppressors of the nimX2(cdc2) mutation of Aspergillus nidulans affect nuclear division, septation and conidiation.Genetics · 2000Article
- The Aspergillus nidulans uvsB gene encodes an ATM-related kinase required for multiple facets of the DNA damage response.Genetics · 2000Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
It is possible to cause G2 arrest in Aspergillus nidulans by inactivating either p34cdc2 or NIMA. We therefore investigated the negative control of these two mitosis-promoting kinases after DNA damage. DNA damage caused rapid Tyr15 phosphorylation of p34cdc2 and transient cell cycle arrest but had little effect on the activity of NIMA. Dividing cells deficient in Tyr15 phosphorylation of p34cdc2 were sensitive to both MMS and UV irradiation and entered lethal premature mitosis with damaged DNA. However, non-dividing quiescent conidiospores of the Tyr15 mutant strain were not sensitive to DNA damage. The UV and MMS sensitivity of cells unable to tyrosine phosphorylate p34cdc2 is therefore caused by defects in DNA damage checkpoint regulation over mitosis. Both the nimA5 and nimT23 temperature-sensitive mutations cause an arrest in G2 at 42 degrees C. Addition of MMS to nimT23 G2-arrested cells caused a marked delay in their entry into mitosis upon downshift to 32 degrees C and this delay was correlated with a long delay in the dephosphorylation and activation of p34cdc2. Addition of MMS to nimA5 G2-arrested cells caused inactivation of the H1 kinase activity of p34cdc2 due to an increase in its Tyr15 phosphorylation level and delayed entry into mitosis upon return to 32 degrees C. However, if Tyr15 phosphorylation of p34cdc2 was prevented then its H1 kinase activity was not inactivated upon MMS addition to nimA5 G2-arrested cells and they rapidly progressed into a lethal mitosis upon release to 32 degrees C. Thus, Tyr15 phosphorylation of p34cdc2 in G2 arrests initiation of mitosis after DNA damage in A. nidulans.
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