Evidence map›Paper›PMID 27798238›Full record

ArticleMolecular biology of the cell2016

LTE1 promotes exit from mitosis by multiple mechanisms.

Jill E Falk, Ian W Campbell, Kelsey Joyce, Jenna Whalen, Anupama Seshan, Angelika Amon

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed.

  1. Article
  2. Meiotic Cytokinesis inJournal of fungi (Basel, Switzerland) · 2024
    Review
  3. The signalling lipid PI3,5POpen biology · 2023
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Cuminal InhibitsMicroorganisms · 2020
    Article
  17. PP2A Functions during Mitosis and Cytokinesis in Yeasts.International journal of molecular sciences · 2019
    Review
  18. Article
  19. Article
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

6 authors.

Jill E FalkDavid H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139.
Ian W CampbellDavid H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139.
Kelsey JoyceDepartment of Biology, Emmanuel College, Boston, MA 02115.
Jenna WhalenDepartment of Biology, Emmanuel College, Boston, MA 02115.
Anupama SeshanDepartment of Biology, Emmanuel College, Boston, MA 02115.
Angelika AmonDavid H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139 angelika@mit.edu.

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
Mitotic exit controlR01HD085866 · NICHD · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI AMON, ANGELIKA B · 2015 to 2019
$1.6M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA014051NICHD NIH HHS R01 HD085866NIGMS NIH HHS T32 GM007287
6 · The paper itself

Abstract

In budding yeast, alignment of the anaphase spindle along the mother-bud axis is crucial for maintaining genome integrity. If the anaphase spindle becomes misaligned in the mother cell compartment, cells arrest in anaphase because the mitotic exit network (MEN), an essential Ras-like GTPase signaling cascade, is inhibited by the spindle position checkpoint (SPoC). Distinct localization patterns of MEN and SPoC components mediate MEN inhibition. Most components of the MEN localize to spindle pole bodies. If the spindle becomes mispositioned in the mother cell compartment, cells arrest in anaphase due to inhibition of the MEN by the mother cell-restricted SPoC kinase Kin4. Here we show that a bud-localized activating signal is necessary for full MEN activation. We identify Lte1 as this signal and show that Lte1 activates the MEN in at least two ways. It inhibits small amounts of Kin4 that are present in the bud via its central domain. An additional MEN-activating function of Lte1 is mediated by its N- and C-terminal GEF domains, which, we propose, directly activate the MEN GTPase Tem1. We conclude that control of the MEN by spindle position is exerted by both negative and positive regulatory elements that control the pathway's GTPase activity.

Indexed as

AnaphaseCell CycleCell Cycle ProteinsCytoskeletal ProteinsGuanine Nucleotide Exchange FactorsMitosisMonomeric GTP-Binding ProteinsProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionSpindle ApparatusSpindle Pole BodiesCell Cycle ProteinsCytoskeletal ProteinsGuanine Nucleotide Exchange FactorsLTE1 protein, S cerevisiaeMonomeric GTP-Binding ProteinsProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsTEM1 protein, S cerevisiae

Identifiers

PMID27798238
PMCPMC5156540

What OpenQuestion holds

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Registered trials

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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.