Evidence map›Paper›PMID 32416080›Full record

ArticleBiophysical journal2020

AimB Is a Small Protein Regulator of Cell Size and MreB Assembly.

John N Werner, Handuo Shi, Jen Hsin, Kerwyn Casey Huang, Zemer Gitai, Eric A Klein

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. 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 at 4 institutions in 1 country.

John N WernerMolecular Biology Department, Princeton University, Princeton, New Jersey.
Handuo ShiDepartment of Bioengineering, Stanford University, Stanford, California.
Jen HsinDepartment of Bioengineering, Stanford University, Stanford, California.
Kerwyn Casey HuangDepartment of Bioengineering, Stanford University, Stanford, California; Department of Microbiology and Immunology, Stanford University, Stanford, California; Chan Zuckerberg Biohub, San Francisco, California.
Zemer GitaiMolecular Biology Department, Princeton University, Princeton, New Jersey.
Eric A KleinDepartment of Biology, Rutgers University-Camden, Camden, New Jersey; Center for Computational and Integrative Biology, Rutgers University-Camden, Camden, New Jersey. Electronic address: eric.a.klein@rutgers.edu.
Princeton University · USStanford University · USChan Zuckerberg Initiative (United States) · USRutgers, The State University of New Jersey · US

Funding

TRAINING & OUTREACH COREP50GM107615 · NIGMS · STANFORD UNIVERSITY · PI FERRELL, JAMES E. · 2013 to 2017
$10.9M
Caulobacter cell shape and cytoskeletal regulationR01GM107384 · NIGMS · PRINCETON UNIVERSITY · PI GITAI, ZEMER · 2013 to 2016
$1.5M
Discovering mechanisms of bacterial cell division: From genotype to phenotypeF32GM100677 · NIGMS · STANFORD UNIVERSITY · PI HSIN, JEN · 2012 to 2014
$78k
NIGMS NIH HHS F32 GM100677NIGMS NIH HHS P50 GM107615NIGMS NIH HHS R01 GM107384
6 · The paper itself

Abstract

The MreB actin-like cytoskeleton assembles into dynamic polymers that coordinate cell shape in many bacteria. In contrast to most other cytoskeleton systems, few MreB-interacting proteins have been well characterized. Here, we identify a small protein from Caulobacter crescentus, an assembly inhibitor of MreB (AimB). AimB overexpression mimics inhibition of MreB polymerization, leading to increased cell width and MreB delocalization. Furthermore, aimB appears to be essential, and its depletion results in decreased cell width and increased resistance to A22, a small-molecule inhibitor of MreB assembly. Molecular dynamics simulations suggest that AimB binds MreB at its monomer-monomer protofilament interaction cleft and that this interaction is favored for C. crescentus MreB over Escherichia coli MreB because of a closer match in the degree of opening with AimB size, suggesting coevolution of AimB with MreB conformational dynamics in C. crescentus. We support this model through functional analysis of point mutants in both AimB and MreB, photo-cross-linking studies with site-specific unnatural amino acids, and species-specific activity of AimB. Together, our findings are consistent with AimB promoting MreB dynamics by inhibiting monomer-monomer assembly interactions, representing a new mechanism for regulating actin-like polymers and the first identification of a non-toxin MreB assembly inhibitor. Because AimB has only 104 amino acids and small proteins are often poorly characterized, our work suggests the possibility of more bacterial cytoskeletal regulators to be found in this class. Thus, like FtsZ and eukaryotic actin, MreB may have a rich repertoire of regulators to tune its precise assembly and dynamics.

Indexed as

Caulobacter crescentusEscherichia coli ProteinsActinsBacterial ProteinsCell SizeCytoskeletonActinsBacterial ProteinsEscherichia coli Proteins

Identifiers

PMID32416080
PMCPMC7399478
OpenAlexW3020947387

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.