Despite intensive research, the role of metabolism in bacterial sporulation remains poorly understood. Here, we demonstrate that sporulation entails a marked metabolic differentiation of the two cells comprising the sporangium: the forespore, which becomes the dormant spore, and the mother cell, which dies as sporulation completes. Our data provide evidence that metabolic precursor biosynthesis becomes restricted to the mother cell and that the forespore becomes reliant on mother cell-derived metabolites for protein synthesis. We further show that arginine is trafficked between the two cells and that proposed proteinaceous channels mediate small-molecule intercellular transport. Thus, sporulation entails the profound metabolic reprogramming of the forespore, which is depleted of key metabolic enzymes and must import metabolites from the mother cell. Together, our results provide a bacterial example analogous to progeny nurturing.
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http://dx.doi.org/10.1126/sciadv.abd6385 | DOI Listing |
J Transl Med
January 2025
State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, School of Medicine, Shanghai East Hospital, Tongji University, Shanghai, 200120, China.
Background: Dilated cardiomyopathy (DCM) is one of the most common causes of heart failure. Infiltration and alterations in non-cardiomyocytes of the human heart involve crucially in the occurrence of DCM and associated immunotherapeutic approaches.
Methods: We constructed a single-cell transcriptional atlas of DCM and normal patients.
J Clin Immunol
January 2025
Population Health Sciences Institute, Newcastle University, Newcastle-Upon-Tyne, UK.
Receptor Interacting Serine/Threonine Kinase 1 (RIPK1) is widely expressed and integral to inflammatory and cell death responses. Autosomal recessive RIPK1-deficiency, due to biallelic loss of function mutations in RIPK1, is a rare inborn error of immunity (IEI) resulting in uncontrolled necroptosis, apoptosis and inflammation. Although hematopoietic stem cell transplantation (HSCT) has been suggested as a potential curative therapy, the extent to which disease may be driven by extra-hematopoietic effects of RIPK1-deficiency, which are non-amenable to HSCT, is not clear.
View Article and Find Full Text PDFCell Tissue Res
January 2025
College of Life Science, Henan Normal University, No. 46, Jianshe Road, Xinxiang 453007, Henan, China.
Sox genes encode a family of transcription factors that regulate multiple biological processes during metazoan development, including embryogenesis, tissue homeostasis, nervous system specification, and stem cell maintenance. The planarian Dugesia japonica contains a reservoir of stem cells that grow and divide continuously to support cellular turnover. However, whether SOX proteins retain these conserved functions in planarians remains to be determined.
View Article and Find Full Text PDFNat Cell Biol
January 2025
Department of Genetics, Yale School of Medicine, New Haven, CT, USA.
Skin epithelial stem cells correct aberrancies induced by oncogenic mutations. Oncogenes invoke different strategies of epithelial tolerance; while wild-type cells outcompete β-catenin-gain-of-function (βcatGOF) cells, Hras cells outcompete wild-type cells. Here we ask how metabolic states change as wild-type stem cells interface with mutant cells and drive different cell-competition outcomes.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Orthopedic Surgery at the First Affiliated Hospital, Harbin Medical University, Harbin, China.
Osteoporosis (OP) is a prevalent age-related bone metabolic disease. Aging and mitochondrial dysfunction are involved in the onset and progression of OP, but the specific mechanisms have not been elucidated. The aim of this study was to identify novel potential biomarkers associated with aging and mitochondria in OP.
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