Evidence map›Paper›PMID 25892235›Full record

ArticleCell reports2015

Host actin polymerization tunes the cell division cycle of an intracellular pathogen.

M Sloan Siegrist, Arjun K Aditham, Akbar Espaillat, Todd A Cameron, Sarah A Whiteside, Felipe Cava, Daniel A Portnoy, Carolyn R Bertozzi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2015. 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
2.9field-weighted citation impact, top 11% 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, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The ever-growing complexity of the mitochondrial fission machinery.Cellular and molecular life sciences : CMLS · 2018
    Review
  6. Article
  7. 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

8 authors at 2 institutions in 2 countries.

M Sloan SiegristDepartment of Chemistry, University of California, Berkeley, Berkeley, CA 94720, USA.
Arjun K AdithamDepartment of Chemistry, University of California, Berkeley, Berkeley, CA 94720, USA.
Akbar EspaillatDepartment of Molecular Biology, Umeå University, Umeå 901 87, Sweden; Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå University, Umeå 901 87, Sweden.
Todd A CameronDepartment of Plant and Microbial Biology, University of California, Berkeley, Berkeley, CA 94720, USA.
Sarah A WhitesideDepartment of Chemistry, University of California, Berkeley, Berkeley, CA 94720, USA.
Felipe CavaDepartment of Molecular Biology, Umeå University, Umeå 901 87, Sweden; Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå University, Umeå 901 87, Sweden.
Daniel A PortnoyDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA; Department of Molecular and Cell Biology, School of Public Health, University of California, Berkeley, Berkeley, CA 94720, USA.
Carolyn R BertozziDepartment of Chemistry, University of California, Berkeley, Berkeley, CA 94720, USA; Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA; Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address: crb@berkeley.edu.
University of California, Berkeley · USUmeå University · SE

Funding

The role of Listeria cyclic-di-AMP during infection and immunityP01AI063302 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI STANLEY, SARAH A · 2004 to 2025
$45.5M
Listeria Hemolysis and Escape From a VacuoleR01AI027655 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI DANIEL A PORTNOY · 1993 to 2026
$10.1M
Mycobacterial Sulfation PathwaysR01AI051622 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI BERTOZZI, CAROLYN · 2002 to 2015
$6.0M
Howard Hughes Medical InstituteNIAID NIH HHS 1P01 AI63302NIAID NIH HHS 1R01 AI051622NIAID NIH HHS 1R01 AI27655NIAID NIH HHS P01 AI063302NIAID NIH HHS R01 AI027655NIAID NIH HHS R01 AI051622
6 · The paper itself

Abstract

Growth and division are two of the most fundamental capabilities of a bacterial cell. While they are well described for model organisms growing in broth culture, very little is known about the cell division cycle of bacteria replicating in more complex environments. Using a D-alanine reporter strategy, we found that intracellular Listeria monocytogenes (Lm) spend a smaller proportion of their cell cycle dividing compared to Lm growing in broth culture. This alteration to the cell division cycle is independent of bacterial doubling time. Instead, polymerization of host-derived actin at the bacterial cell surface extends the non-dividing elongation period and compresses the division period. By decreasing the relative proportion of dividing Lm, actin polymerization biases the population toward cells with the highest propensity to form actin tails. Thus, there is a positive-feedback loop between the Lm cell division cycle and a physical interaction with the host cytoskeleton.

Indexed as

Cell DivisionPolymerizationActin CytoskeletonActinsAnimalsCell LineFeedback, PhysiologicalHost-Pathogen InteractionsListeria monocytogenesMacrophagesMiceActins

Identifiers

PMID25892235
PMCPMC4417095
OpenAlexW2026448481

What OpenQuestion holds

Textmetadata
LicenceTDM
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.