Evidence map›Paper›PMID 26715672›Full record

ArticleGenetics2016

Evidence That an Unconventional Actin Can Provide Essential F-Actin Function and That a Surveillance System Monitors F-Actin Integrity in Chlamydomonas.

Masayuki Onishi, John R Pringle, Frederick R Cross

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Actin cytoskeletal regulation of ciliogenesis in development and disease.Developmental dynamics : an official publication of the American Association of Anatomists · 2024
    Review
  5. Dramatic changes in mitochondrial subcellular location and morphology accompany activation of the COProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Review
  7. Article
  8. Initial ciliary assembly inMolecular biology of the cell · 2023
    Article
  9. Review
  10. Article
  11. Review
  12. Finding your unique path in science.Molecular biology of the cell · 2020
    Article
  13. Article
  14. Cleavage-furrow formation without F-actin inProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Review
  16. Profilin choreographs actin and microtubules in cells and cancer.International review of cell and molecular biology · 2020
    Article
  17. Molecular biology of the cell · 2019
    Article
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Masayuki OnishiDepartment of Genetics, Stanford University School of Medicine, Stanford, California 94305.
John R PringleDepartment of Genetics, Stanford University School of Medicine, Stanford, California 94305 jpringle@stanford.edu fcross@mail.rockefeller.edu.
Frederick R CrossThe Rockefeller University, New York, New York 10065 jpringle@stanford.edu fcross@mail.rockefeller.edu.
Stanford University · USRockefeller University · US

Funding

Sources and Consequences of noise in cell cycle regulationR01GM078153 · NIGMS · ROCKEFELLER UNIVERSITY · PI CROSS, FREDERICK R. · 2006 to 2019
$3.3M
NIGMS NIH HHS 5R01GM078153-07NIGMS NIH HHS R01 GM078153
6 · The paper itself

Abstract

Actin is one of the most conserved eukaryotic proteins. It is thought to have multiple essential cellular roles and to function primarily or exclusively as filaments ("F-actin"). Chlamydomonas has been an enigma, because a null mutation (ida5-1) in its single gene for conventional actin does not affect growth. A highly divergent actin gene, NAP1, is upregulated in ida5-1 cells, but it has been unclear whether NAP1 can form filaments or provide actin function. Here, we used the actin-depolymerizing drug latrunculin B (LatB), the F-actin-specific probe Lifeact-Venus, and genetic and molecular methods to resolve these issues. LatB-treated wild-type cells continue to proliferate; they initially lose Lifeact-stained structures but recover them concomitant with upregulation of NAP1. Thirty-nine LatB-sensitive mutants fell into four genes (NAP1 and LAT1-LAT3) in which we identified the causative mutations using a novel combinatorial pool-sequencing strategy. LAT1-LAT3 are required for NAP1 upregulation upon LatB treatment, and ectopic expression of NAP1 largely rescues the LatB sensitivity of the lat1-lat3 mutants, suggesting that the LAT gene products comprise a regulatory hierarchy with NAP1 expression as the major functional output. Selection of LatB-resistant revertants of a nap1 mutant yielded dominant IDA5 mutations that presumably render F-IDA5 resistant to LatB, and nap1 and lat mutations are synthetically lethal with ida5-1 in the absence of LatB. We conclude that both IDA5 and the divergent NAP1 can form filaments and redundantly provide essential F-actin functions and that a novel surveillance system, probably responding to a loss of F-actin, triggers NAP1 expression and perhaps other compensatory responses.

Indexed as

Actin CytoskeletonActinsAlgal ProteinsAllelesBridged Bicyclo Compounds, HeterocyclicChlamydomonas reinhardtiiSynthetic Lethal MutationsThiazolidinesUp-RegulationActinsAlgal ProteinsBridged Bicyclo Compounds, Heterocycliclatrunculin BThiazolidinesactinalgal and plant cytoskeletonsChlamydomonaslatrunculinmutation identification by sequencing

Identifiers

PMID26715672
PMCPMC4788133
OpenAlexW2208056585

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.