Evidence map›Paper›PMID 10198005›Full record

ArticleJournal of bacteriology1999

The CtrA response regulator mediates temporal control of gene expression during the Caulobacter cell cycle.

A Reisenauer, K Quon, L Shapiro

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of bacteriology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 128 citations in OpenAlex.

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  2. Proceedings of the National Academy of Sciences of the United States of America · 2025
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  12. Cargo competition for a dimerization interface restricts and stabilizes a bacterial protease adaptor.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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 1 institution in 1 country.

A ReisenauerDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305-5329, USA. reisen@cmgm.stanford.edu
K Quon
L Shapiro
Stanford University · US

Funding

REGULATION OF DIFFERENTIATION IN CAULOBACTERR01GM032506 · NIGMS · YESHIVA UNIVERSITY · PI SHAPIRO, LUCILLE · 1985 to 2014
$7.1M
DEVELOPMENT CONTROL OF DNA REPLICATION IN CAULOBACTERR01GM051426 · NIGMS · STANFORD UNIVERSITY · PI SHAPIRO, LUCILLE · 1994 to 2013
$3.8M
REGULATION OF DIFFERENTIATION IN CAULOBACTERR37GM032506 · NIGMS · STANFORD UNIVERSITY · PI SHAPIRO, LUCILLE · 1993 to 2002
$1.4M
NIGMS NIH HHS GM 32506/5120MZNIGMS NIH HHS GM 51426NIGMS NIH HHS R01 GM032506NIGMS NIH HHS R01 GM051426NIGMS NIH HHS R37 GM032506
6 · The paper itself

Abstract

In its role as a global response regulator, CtrA controls the transcription of a diverse group of genes at different times in the Caulobacter crescentus cell cycle. To understand the differential regulation of CtrA-controlled genes, we compared the expression of two of these genes, the fliQ flagellar gene and the ccrM DNA methyltransferase gene. Despite their similar promoter architecture, these genes are transcribed at different times in the cell cycle. PfliQ is activated earlier than PccrM. Phosphorylated CtrA (CtrA approximately P) bound to the CtrA recognition sequence in both promoters but had a 10- to 20-fold greater affinity for PfliQ. This difference in affinity correlates with temporal changes in the cellular levels of CtrA. Disrupting a unique inverted repeat element in PccrM significantly reduced promoter activity but not the timing of transcription initiation, suggesting that the inverted repeat does not play a major role in the temporal control of ccrM expression. Our data indicate that differences in the affinity of CtrA approximately P for PfliQ and PccrM regulate, in part, the temporal expression of these genes. However, the timing of fliQ transcription but not of ccrM transcription was altered in cells expressing a stable CtrA derivative, indicating that changes in CtrA approximately P levels alone cannot govern the cell cycle transcription of these genes. We propose that changes in the cellular concentration of CtrA approximately P and its interaction with accessory proteins influence the temporal expression of fliQ, ccrM, and other key cell cycle genes and ultimately the regulation of the cell cycle.

Indexed as

DNA-Binding ProteinsGene Expression Regulation, BacterialMembrane ProteinsTranscription FactorsBacterial ProteinsBase SequenceCaulobacter crescentusCell CycleMolecular Sequence DataPhosphoproteinsPhosphorylationProtein BindingRegulatory Sequences, Nucleic AcidSite-Specific DNA-Methyltransferase (Adenine-Specific)Time FactorsBacterial ProteinsCtrA protein, CaulobacterDNA-Binding ProteinsDNA modification methylase CcrMFliQ protein, BacteriaMembrane ProteinsPhosphoproteinsSite-Specific DNA-Methyltransferase (Adenine-Specific)Transcription Factors

Identifiers

PMID10198005
PMCPMC93667
OpenAlexW2131288254

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.