ArticleCytoskeleton (Hoboken, N.J.)2019
A requirement for septins and the autophagy receptor p62 in the proliferation of intracellular Shigella.
Article in Cytoskeleton (Hoboken, N.J.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Cytoskeleton-mediated autophagy regulation in neuroimmune contexts: molecular mechanisms and functional perspectives.Frontiers in immunology · 2026Review
- Septins modulate the autophagy response after nutrient starvation.Molecular biology of the cell · 2024Article
- Measles virus-imposed remodeling of the autophagy machinery determines the outcome of bacterial coinfection.Autophagy · 2023Article
- The versatile defender: exploring the multifaceted role of p62 in intracellular bacterial infection.Frontiers in cellular and infection microbiology · 2023Review
- Capsaicin InhibitsFrontiers in pharmacology · 2022Article
- The pentose phosphate pathway constitutes a major metabolic hub in pathogenic Francisella.PLoS pathogens · 2021Article
- SEPT7 Interacts with KIF20A and Regulates the Proliferative State of Neural Progenitor Cells During Cortical Development.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Injury and Apoptosis in the Palatopharyngeal Muscle in Patients with Obstructive Sleep Apnea-Hypopnea Syndrome.Medical science monitor : international medical journal of experimental and clinical research · 2020Observational
- Septin-2 is overexpressed in epithelial ovarian cancer and mediates proliferation via regulation of cellular metabolic proteins.Oncotarget · 2019Article
- A requirement for septins and the autophagy receptor p62 in the proliferation of intracellular Shigella.Cytoskeleton (Hoboken, N.J.) · 2019Article
- Septins promote caspase activity and coordinate mitochondrial apoptosis.Cytoskeleton (Hoboken, N.J.)Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Shigella flexneri, a Gram-negative enteroinvasive pathogen, causes inflammatory destruction of the human intestinal epithelium. During infection of epithelial cells, Shigella escape from the phagosome to the cytosol, where they reroute host cell glycolysis to obtain nutrients for proliferation. Septins, a poorly understood component of the cytoskeleton, can entrap cytosolic Shigella targeted to autophagy in cage-like structures to restrict bacterial proliferation. Although bacterial entrapment by septin caging has been the subject of intense investigation, the role of septins and the autophagy machinery in the proliferation of noncaged Shigella is mostly unknown. Here, we found that intracellular Shigella fail to efficiently proliferate in SEPT2-, SEPT7-, or p62/SQSTM1-depleted cells. Consistent with a failure to proliferate, single cell analysis of bacteria not entrapped in septin cages showed that the number of metabolically active Shigella in septin- or p62-depleted cells is reduced. Targeted metabolomic analysis revealed that host cell glycolysis is dysregulated in septin-depleted cells, suggesting a key role for septins in modulation of glycolysis. Together, these results suggest that septins and the autophagy machinery may regulate metabolic pathways that promote the proliferation of intracellular Shigella not entrapped in septin cages.
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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.