Evidence map›Paper›PMID 25385627›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Single mutations in sasA enable a simpler ΔcikA gene network architecture with equivalent circadian properties.

Ryan K Shultzaberger, Joseph S Boyd, Takeo Katsuki, Susan S Golden, Ralph J Greenspan

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Discrete gene replication events drive coupling between the cell cycle and circadian clocks.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  6. Circadian Rhythms in Cyanobacteria.Microbiology and molecular biology reviews : MMBR · 2015
    Review
  7. Review
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

5 authors at 2 institutions in 2 countries.

Ryan K ShultzabergerCenter for Circadian Biology and Kavli Institute for Brain and Mind, University of California, San Diego, La Jolla, CA 92093-0116.
Joseph S BoydCenter for Circadian Biology and.
Takeo KatsukiKavli Institute for Brain and Mind, University of California, San Diego, La Jolla, CA 92093-0116.
Susan S GoldenCenter for Circadian Biology and sgolden@ucsd.edu rgreenspan@ucsd.edu.
Ralph J GreenspanCenter for Circadian Biology and Kavli Institute for Brain and Mind, University of California, San Diego, La Jolla, CA 92093-0116 sgolden@ucsd.edu rgreenspan@ucsd.edu.
Canadian Sleep & Circadian Network · CAUniversity of California, San Diego · US

Funding

THE PATHWAY THAT SETS THE CYANOBACTERIAL CIRCADIAN CLOCKR01GM062419 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GOLDEN, SUSAN S · 2001 to 2015
$3.9M
The properties and evolvability of the cyanobacterial circadian genetic networkF32GM097977 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHULTZABERGER, RYAN K · 2012 to 2013
$106k
NIGMS NIH HHS F32 GM097977NIGMS NIH HHS GM097977-01A1NIGMS NIH HHS R01 GM062419NIGMS NIH HHS R01GM062419
6 · The paper itself

Abstract

The circadian input kinase of the cyanobacterium Synechococcus elongatus PCC 7942 (CikA) is important both for synchronizing circadian rhythms with external environmental cycles and for transferring temporal information between the oscillator and the global transcriptional regulator RpaA (regulator of phycobilisome-associated A). KOs of cikA result in one of the most severely altered but still rhythmic circadian phenotypes observed. We chemically mutagenized a cikA-null S. elongatus strain and screened for second-site suppressor mutations that could restore normal circadian rhythms. We identified two independent mutations in the Synechococcus adaptive sensor A (sasA) gene that produce nearly WT rhythms of gene expression, likely because they compensate for the loss of CikA on the temporal phosphorylation of RpaA. Additionally, these mutations restore the ability to reset the clock after a short dark pulse through an output-independent pathway, suggesting that SasA can influence entrainment through direct interactions with KaiC, a property previously unattributed to it. These experiments question the evolutionary advantage of integrating CikA into the cyanobacterial clock, challenge the conventional construct of separable input and output pathways, and show how easily the cell can adapt to restore phenotype in a severely compromised genetic network.

Indexed as

Circadian RhythmGene Regulatory NetworksGenes, BacterialPoint MutationBacterial ProteinsPolymorphism, GeneticProtein KinasesSynechococcusBacterial ProteinsCikA protein, bacteriaProtein Kinasescyanobacteriaevolutiongene network

Identifiers

PMID25385627
PMCPMC4250164
OpenAlexW1965643809

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.