ArticleMolecular & cellular proteomics : MCP2026
Sec and Tat Mediated Secretion Safeguards Mycobacterium tuberculosis Membrane Homeostasis.
Article in Molecular & cellular proteomics : MCP, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein secretion is essential for the growth and virulence of Mycobacterium tuberculosis, yet the organization and function of its secretion pathways remain poorly understood. We reviewed the existing literature, combined it with systematic queries, and finalized annotations based on experimental data and computational predictions to compile a curated list of 92 secretory components and 198 reactions involved in Sec, twin-arginine translocation (Tat), and ESX pathways. Using CRISPRi, targeted depletion of SecA1 or TatAC impaired both in vitro growth and ex vivo survival. Label-free quantitative secretome analysis revealed decreased export of substrates dependent on SecA1 and TatAC, with enrichment of cytosolic proteins in culture filtrates, indicating increased membrane dysbiosis. Membrane proteomics showed elevated levels of proteins engaged in intermediary and lipid metabolism, while proteins associated with the cell wall and cell processes decreased, suggesting weakened membrane integrity. Loss of SecA1 or TatAC increased membrane permeability, with the effect being more pronounced in the case of TatAC, and caused structural abnormalities seen under electron microscopy. Overall, our integrated multi-omics and functional genetics studies demonstrate that the SecA1 and Tat pathways are essential for maintaining membrane homeostasis in Mycobacterium tuberculosis. These results suggest that essential secretory proteins may be promising targets for therapeutic intervention.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.