Another two genes controlling mitotic intragenic recombination and recovery from UV damage in Aspergillus nidulans III. Photoreactivition of UV damage in uvsD and uvsE mutants

Fortuin, J.J.H.

doi:10.1016/0027-5107(71)90005-4

Cited by 10 publications

(3 citation statements)

References 11 publications

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“…In addition, these two checkpoint mechanisms may actually overlap as they both monitor, and respond to, the state of DNA, and therefore may share common components of a checkpoint signal transduction pathway leading to Tyr15 phosphorylation of p34 cdc2 . This hypothesis is supported by the observations that A.nidulans cells bearing mutations in uvsB or uvsD , which were originally isolated as UV irradiation‐sensitive mutants (Jansen, 1970; Fortuin, 1971), are deficient not only in S‐phase checkpoint control but also in the G 2 /M DNA damage checkpoint control (X.Ye, A.Tang, R.Fincher and S.Osmani, unpublished results). Similarly, several genes have been identified in fission yeasts that are required for both S‐phase and G 2 /M checkpoint controls (Carr, 1995) and these functions may also influence the Tyr15 phosphorylation state of p34 cdc2 , although this has not as yet been tested.…”

Section: Discussionmentioning

confidence: 68%

The G2/M DNA damage checkpoint inhibits mitosis through Tyr15 phosphorylation of p34cdc2 in Aspergillus nidulans

Fincher

Tang

et al. 1997

The EMBO Journal

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It is possible to cause G2 arrest in Aspergillus nidulansby 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°C. Addition of MMS to nimT23 G2‐arrested cells caused a marked delay in their entry into mitosis upon downshift to 32°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°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°C. Thus, Tyr15 phosphorylation of p34cdc2 in G2 arrests initiation of mitosis after DNA damage in A.nidulans.

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Section: Discussionmentioning

confidence: 68%

The G2/M DNA damage checkpoint inhibits mitosis through Tyr15 phosphorylation of p34cdc2 in Aspergillus nidulans

Fincher

Tang

et al. 1997

The EMBO Journal

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“…With the total genome sequence available, it will now be possible to analyse all components of pathways or complexes and their interactions, and also to obtain disruption or deletion strains of all genes of interest, including the genes for well-characterized mutants involved in DNA repair [e.g., the uvsE gene of Fortuin (1971) which is closely related and epistatic with uvsC RAD51 and shows similar effects on recombination but not on mutation (E. Kafer and S.-K. Chae, unpublished observations)]. …”

Section: Perspectivesmentioning

confidence: 99%

Aspergillus nidulans as a model system to characterize the DNA damage response in eukaryotes

Goldman

Käfer

2004

Fungal Genetics and Biology

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“…UV irradiation and MMS treatment UV survival was determined as described by Fortuin (1970), with minor modi®cations: spores were plated (in triplicate) on CM in three concentrations (between 10 6 and 10 2 spores/plate). After preincubation for 6 h at 37°C, the plates were UV irradiated (18 erg/mm 2 /s) for various periods of time (up to 90 s).…”

Section: Northern Blot Analysismentioning

confidence: 99%

Cloning, sequencing, disruption and phenotypic analysis of uvsC, an Aspergillus nidulans homologue of yeast RAD51

et al. 1997

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We have cloned the uvsC gene of Aspergillus nidulans by complementation of the A. nidulans uvsC114 mutant. The predicted protein UVSC shows 67.4% sequence identity to the Saccharomyces cerevisiae Rad51 protein and 27.4% sequence identity to the Escherichia coli RecA protein. Transcription of uvsC is induced by methyl-methane sulphonate (MMS), as is transcription of RAD51 of yeast. Similar levels of uvsC transcription were observed after MMS induction in a uvsC+ strain and the uvsC114 mutant. The coding sequence of the uvsC114 allele has a deletion of 6 bp, which results in deletion of two amino acids and replacement of one amino acid in the translation product. In order to gain more insight into the biological function of the uvsC gene, a uvsC null mutant was constructed, in which the entire uvsC coding sequence was replaced by a selectable marker gene. Meiotic and mitotic phenotypes of a uvsC+ strain, the uvsC114 mutant and the uvsC null mutant were compared. The uvsC null mutant was more sensitive to both UV and MMS than the uvsC114 mutant. The uvsC114 mutant arrested in meiotic prophase-I. The uvsC null mutant arrested at an earlier stage, before the onset of meiosis. One possible interpretation of these meiotic phenotypes is that the A. nidulans homologue of Rad51 of yeast has a role both in the specialized processes preceding meiosis and in meiotic prophase I.

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Another two genes controlling mitotic intragenic recombination and recovery from UV damage in Aspergillus nidulans III. Photoreactivition of UV damage in uvsD and uvsE mutants

Cited by 10 publications

References 11 publications

The G2/M DNA damage checkpoint inhibits mitosis through Tyr15 phosphorylation of p34cdc2 in Aspergillus nidulans

The G2/M DNA damage checkpoint inhibits mitosis through Tyr15 phosphorylation of p34cdc2 in Aspergillus nidulans

Aspergillus nidulans as a model system to characterize the DNA damage response in eukaryotes

Cloning, sequencing, disruption and phenotypic analysis of uvsC, an Aspergillus nidulans homologue of yeast RAD51

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