Evidence map›Paper›PMID 17703305›Full record

ArticleCurrent genetics2007

Neurosprora crassa RAD5 homologue, mus-41, inactivation results in higher sensitivity to mutagens but has little effect on PCNA-ubiquitylation in response to UV-irradiation.

Tsuyoshi Kawabata, Akihiro Kato, Keiichiro Suzuki, Hirokazu Inoue

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Article in Current genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Tsuyoshi KawabataDepartment of Regulation Biology, Saitama University, Sakura-ku Shimo-ookubo 255, Saitama city, Saitama 338-8570, Japan. hinoue@post.saitama-u.ac.jp
Akihiro Kato
Keiichiro Suzuki
Hirokazu Inoue

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA replication machinery stalls at damaged sites on DNA. Postreplicaton repair (PRR) is a system to avoid cell death in such circumstances of deadlock. In Saccharomyces cerevisiae, the Rad6/Rad18 heterodimer plays pivotal roles in PRR. It promotes translesion synthesis via the monoubiquitylation of the DNA sliding clamp, PCNA. Ubc13/Mms2/Rad5 can extend the ubiquitin chain from this monoubiquitylated PCNA with a non-canonical lysine 63-linked ubiquitin-chain, resulting in an error-free mode of bypass. In this study, we identified and characterized the RAD5 homolog in Neurospora crassa, which we named mus-41. A mus-41 mutant was sensitive to several DNA-damaging agents including UV and MMS. Genetic analyses indicated that uvs-2 (RAD18 homolog) was epistatic to mus-41, suggesting a role for mus-41 in postreplication repair. Additionally, it was shown that mus-41 has a role independent from TLS gene upr-1 (REV3 homolog) and works in the error-free pathway, indicating that the function of mus-41 as a RAD5 homolog is also conserved in N. crassa. However, mus-41 is not essential for the ubiquitylation of PCNA that is detected in the wild-type background, suggesting that there is another ubiquitin ligase catalyzing ubiquitylation of PCNA in response to UV in N. crassa.

Indexed as

Adenosine TriphosphatasesAmino Acid SequenceBlotting, WesternDNA DamageDNA RepairDNA ReplicationFungal ProteinsGene Expression Regulation, FungalMethyl MethanesulfonateMolecular Sequence DataMutagensNeurospora crassaProliferating Cell Nuclear AntigenSequence Homology, Amino AcidUbiquitinUbiquitin-Conjugating EnzymesAdenosine TriphosphatasesFungal ProteinsMethyl MethanesulfonateMutagensProliferating Cell Nuclear AntigenUbiquitinUbiquitin-Conjugating Enzymes

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.