ArticleMolecular biology of the cell1999
Liz1p, a novel fission yeast membrane protein, is required for normal cell division when ribonucleotide reductase is inhibited.
Article in Molecular biology of the cell, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Inner nuclear membrane protein Lem2 facilitates Rad3-mediated checkpoint signaling under replication stress induced by nucleotide depletion in fission yeast.Cellular signalling · 2016Article
- TORC2 is required to maintain genome stability during S phase in fission yeast.The Journal of biological chemistry · 2013Article
- Global fitness profiling of fission yeast deletion strains by barcode sequencing.Genome biology · 2010Article
- TOR complex 2 controls gene silencing, telomere length maintenance, and survival under DNA-damaging conditions.Molecular and cellular biology · 2009Article
- Involvement of fission yeast Clr6-HDAC in regulation of the checkpoint kinase Cds1.Nucleic acids research · 2008Article
- Cell division defects of Schizosaccharomyces pombe liz1- mutants are caused by defects in pantothenate uptake.Eukaryotic cell · 2004Article
- Identification of ribonucleotide reductase protein R1 as an activator of microtubule nucleation in Xenopus egg mitotic extracts.Molecular biology of the cell · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ribonucleotide reductase activity is required for generating deoxyribonucleotides for DNA replication. Schizosaccharomyces pombe cells lacking ribonucleotide reductase activity arrest during S phase of the cell cycle. In a screen for hydroxyurea-sensitive mutants in S. pombe, we have identified a gene, liz1(+), which when mutated reveals an additional, previously undescribed role for ribonucleotide reductase activity during mitosis. Inactivation of ribonucleotide reductase, by either hydroxyurea or a cdc22-M45 mutation, causes liz1(-) cells in G2 to undergo an aberrant mitosis, resulting in chromosome missegregation and late mitotic arrest. liz1(+) encodes a 514-amino acid protein with strong similarity to a family of transmembrane transporters, and localizes to the plasma membrane of the cell. These results reveal an unexpected G2/M function of ribonucleotide reductase and establish that defects in a transmembrane protein can affect cell cycle progression.
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Registered trials
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.