Evidence map›Paper›PMID 14527997›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

SecA2-dependent secretion of autolytic enzymes promotes Listeria monocytogenes pathogenesis.

Laurel L Lenz, Sina Mohammadi, Aimee Geissler, Daniel A Portnoy

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
12.7field-weighted citation impact, top 1% 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

120 citing papers in PubMed, 290 citations in OpenAlex.

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  10. Leucine-rich repeat proteins ofFrontiers in microbiology · 2024
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  11. Pathogens (Basel, Switzerland) · 2022
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  16. Different Shades ofFrontiers in microbiology · 2021
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  18. The Structure ofInternational journal of molecular sciences · 2020
    Article
  19. Article
  20. Review

60 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Laurel L LenzDepartment of Molecular and Cell Biology, University of California, 401 Barker Hall, Berkeley, CA 94720-3202, USA. lenz@uclink4.berkeley.edu
Sina Mohammadi
Aimee Geissler
Daniel A Portnoy
University of California, Berkeley · US

Funding

Listeria Hemolysis and Escape From a VacuoleR01AI027655 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI DANIEL A PORTNOY · 1993 to 2026
$10.1M
ACTA AND THE CELL TO CELL SPREAD OF LISTERIAR37AI029619 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI PORTNOY, DANIEL A · 1995 to 2004
$1.8M
PHASE VARIATION IN LISTERIA MONOCYTOGENESF32AI010481 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI LENZ, LAUREL L · 2000 to 2002
$119k
MOLECULAR BIOLOGY OF LISTERIA-HOST CELL INTERACTIONR01AI029619 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI PORTNOY, DANIEL A · 1990 to 1994
–
LISTERIA HEMOLYSIN AND INTRACELLULAR GROWTHR29AI027655 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI PORTNOY, DANIEL A · 1988 to 1992
–
NIAID NIH HHS AI 10481NIAID NIH HHS AI 27655NIAID NIH HHS AI 29619NIAID NIH HHS F32 AI010481NIAID NIH HHS R01 AI027655NIAID NIH HHS R37 AI029619
6 · The paper itself

Abstract

Pathogenic bacteria secrete proteins that promote invasion of host tissues and resistance to immune responses. However, secretion mechanisms that contribute to the enormous morbidity and mortality of Gram-positive bacteria are largely undefined. An auxiliary protein secretion system (SecA2) has recently emerged in Listeria monocytogenes and eight other Gram-positive pathogens. Here, a proteomics approach identified seventeen SecA2-dependent secreted and surface proteins of L. monocytogenes, the two most abundant of which [the p60 and N-acetylmuramidase (NamA) autolysins] hydrolyze bacterial peptidoglycan (PGN) and contribute to host colonization. SecA2-deficient (DeltaSecA2) bacteria were rapidly cleared after systemic infection of murine hosts, and in cultured cells showed reduced cell-cell spread. p60 or NamA deficiencies (Deltap60 and DeltaNamA) caused intermediate reductions in bacterial virulence in vivo, yet showed no defect for infection of cultured cells. Restoration of virulence in Deltap60 bacteria required full-length p60 with an intact catalytic domain, suggesting that PGN hydrolysis by p60 is crucial for L. monocytogenes virulence. Coordinated PGN hydrolysis by p60 and NamA activities is predicted to generate a muramyl glycopeptide, glucosaminylmuramyl dipeptide (GMDP), which is known to modify host inflammatory responses. Thus, SecA2-dependent secretion may promote release of muramyl peptides that subvert host pattern recognition.

Indexed as

Adenosine TriphosphatasesAnimalsAutolysisBacterial ProteinsCells, CulturedEscherichia coli ProteinsListeria monocytogenesMacrophagesMembrane Transport ProteinsMiceMice, Inbred BALB CN-Acetylmuramoyl-L-alanine AmidasePeptidoglycanProteomicsSecA ProteinsSEC Translocation ChannelsAdenosine TriphosphatasesBacterial ProteinsEscherichia coli ProteinsMembrane Transport ProteinsN-Acetylmuramoyl-L-alanine AmidasePeptidoglycanSecA ProteinsSEC Translocation Channels

Identifiers

PMID14527997
PMCPMC218775
OpenAlexW2035295085

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.