A growing bacterium typically divides into two genetically identical and morphologically similar sister cells and eventually gives rise to a clonal population. Nevertheless, significant phenotypic differentiation among isogenic cells frequently occurs, with the resulting heterogeneity in cellular behavior often ensuring population level growth and survival in complex and unpredictable environments. Although several mechanisms underlying the generation of phenotypic heterogeneity have been elucidated, the speed with which identical sister cells tend to phenotypically diverge from each other has so far remained unaddressed. Using Escherichia coli as a model organism, we therefore examined the timing and dynamics of phenotypic individualization among sister cells by scrutinizing and modeling microscopically tracked clonally growing populations before and after a semi-lethal heat challenge. This analysis revealed that both survival probability and post-stress physiology of sister cells shift from highly similar to uncorrelated within the first decile of their cell cycles. This nearly-immediate post-fission randomization of sister cell fates highlights the potential of stochastic fluctuations during clonal growth to rapidly generate phenotypically independent individuals.
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http://dx.doi.org/10.1038/s41598-017-08660-0 | DOI Listing |
Nucleic Acids Res
January 2025
Laboratoire de Microbiologie et de Génétique Moléculaires, Centre de Biologie Intégrative, Université de Toulouse, CNRS, 165 Rue Marianne Grunberg-Manago, campus Paul Sabatier, 118, route de Narbonne, 31062, Toulouse Cedex, France.
Bacterial genomes contain a plethora of secondary replicons of divergent size. Circular replicons must carry a system for resolving dimeric forms, resulting from recombination between sister copies. These systems use site-specific recombinases.
View Article and Find Full Text PDFMol Oncol
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Department of Oral Pathology, College of Dentistry, Gangneung-Wonju National University, Korea.
The dynamics of focal adhesions (FAs) are essential physiological processes involved in cell spreading, metastasis, and regulation of the actin cytoskeleton. FAs are complex structures comprising proteins, such as paxillin and zyxin, which interact with extracellular membranes and influence cell motility and morphology. Although related studies have been reported in various cancers, the function and molecular mechanisms of oral squamous cell carcinoma (OSCC) remain unknown.
View Article and Find Full Text PDFCommun Med (Lond)
January 2025
Department of Pediatrics, Division of Blood and Marrow Transplantation, University of Minnesota, Minneapolis, MN, USA.
Background: Multiple sulfatase deficiency (MSD) is an exceptionally rare neurodegenerative disorder due to the absence or deficiency of 17 known cellular sulfatases. The activation of all these cellular sulfatases is dependent on the presence of the formylglycine-generating enzyme, which is encoded by the SUMF1 gene. Disease-causing homozygous or compound heterozygous variants in SUMF1 result in MSD.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Life Science and Medical Bioscience, Laboratory of Cytoskeletal Logistics, Graduate School of Advanced Science and Engineering, Waseda University, Shinjuku, Tokyo, Japan.
In mammalian epithelial cells, cytoplasmic microtubules are mainly non-centrosomal, through the functions of the minus-end binding proteins CAMSAP2 and CAMSAP3. When cells enter mitosis, cytoplasmic microtubules are reorganized into the spindle composed of both centrosomal and non-centrosomal microtubules. The function of the CAMSAP proteins upon spindle assembly remains unknown, as these do not exhibit evident localization to spindle microtubules.
View Article and Find Full Text PDFLife Sci Alliance
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https://ror.org/01kj2bm70 Mitochondrial Research Group, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK
Pathogenic variants in cytochrome oxidase assembly factor 5 (COA5), a proposed complex IV (CIV) assembly factor, have been shown to cause clinical mitochondrial disease with two siblings affected by neonatal hypertrophic cardiomyopathy manifesting a rare, homozygous missense variant (NM_001008215.3: c.157G>C, p.
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