ArticleThe Journal of cell biology2010
Phosphorylation of Lte1 by Cdk prevents polarized growth during mitotic arrest in S. cerevisiae.
Article in The Journal of cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Cla4 phosphorylates histone methyltransferase Set1 to prevent its degradation by the APC/CScience advances · 2023Article
- Phosphorylation of RGS regulates MAP kinase localization and promotes completion of cytokinesis.Life science alliance · 2022Article
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- Haspin regulates Ras localization to promote Cdc24-driven mitotic depolarization.Cell discovery · 2020Article
- gRASping Depolarization: Contribution of RAS GTPases to Mitotic Polarity Clusters Resolution.Frontiers in cell and developmental biology · 2020Article
- Temporal and compartment-specific signals coordinate mitotic exit with spindle position.Nature communications · 2017Article
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- Spatially distinct functions of Clb2 in the DNA damage response.Cell cycle (Georgetown, Tex.) · 2014Article
- Dissection of Cdk1-cyclin complexes in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Budding yeast ATM/ATR control meiotic double-strand break (DSB) levels by down-regulating Rec114, an essential component of the DSB-machinery.PLoS genetics · 2013Article
- A dynamical model of the spindle position checkpoint.Molecular systems biology · 2012Article
- Ras-Mediated Signal Transduction and Virulence in Human Pathogenic Fungi.Fungal genomics & biology · 2012Article
- Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Lte1 is known as a regulator of mitotic progression in budding yeast. Here we demonstrate phosphorylation-dependent inhibition of polarized bud growth during G2/M by Lte1. Cla4 activity first localizes Lte1 to the polarity cap and thus specifically to the bud. This localization is a prerequisite for subsequent Clb-Cdk-dependent phosphorylation of Lte1 and its relocalization to the entire bud cortex. There, Lte1 interferes with activation of the small GTPases, Ras and Bud1. The inhibition of Bud1 prevents untimely polarization until mitosis is completed and Cdc14 phosphatase is released. Inhibition of Bud1 and Ras depends on Lte1's GEF-like domain, which unexpectedly inhibits these small G proteins. Thus, Lte1 has dual functions for regulation of mitotic progression: it both induces mitotic exit and prevents polarized growth during mitotic arrest, thereby coupling cell cycle progression and morphological development.
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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.