Asymmetric cell division is the primary mechanism to generate cellular diversity, and it relies on the correct partitioning of cell fate determinants. However, the mechanism by which these determinants are delivered and positioned is poorly understood, and the upstream signal to initiate asymmetric cell division is unknown. Here we report that the endoplasmic reticulum (ER) is asymmetrically partitioned during mitosis in epithelial cells just before delamination and selection of a proneural cell fate in the early embryo. At the start of gastrulation, the ER divides asymmetrically into a population of asynchronously dividing cells at the anterior end of the embryo. We found that this asymmetric division of the ER depends on the highly conserved ER membrane protein Jagunal (Jagn). RNA inhibition of just before the start of gastrulation disrupts this asymmetric division of the ER. In addition, -deficient embryos display defects in apical-basal spindle orientation in delaminated embryonic neuroblasts. Our results describe a model in which an organelle is partitioned asymmetrically in an otherwise symmetrically dividing cell population just upstream of cell fate determination and updates previous models of spindle-based selection of cell fate during mitosis.
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http://dx.doi.org/10.1091/mbc.E16-09-0690 | DOI Listing |
Int J Biol Macromol
December 2024
State Key Laboratory of Swine and Poultry Breeding Industry & Guangdong Key Laboratory of Animal Breeding and Nutrition & Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China. Electronic address:
The faithful production of primordial germ cells (PGCs) in vitro opens a wide range of novel applications in reproductive biology and medicine. However, the reproducibility of PGCs culture conditions across different laboratories or breeds remains a challenge. Therefore, it is necessary to research the molecular dynamics that lead to the gradual establishment of cultured PGCs lines network.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Translational Medical Sciences, School of Medicine, Texas A&M Health Science Center, Texas A&M University, Houston, TX 77030.
Induction of cell fates by growth factors impacts many facets of developmental biology and disease. LIN-3/EGF induces the equipotent vulval precursor cells (VPCs) in to assume the 3˚-3˚-2˚-1˚-2˚-3˚ pattern of cell fates. 1˚ and 2˚ cells become specialized epithelia and undergo stereotyped series of cell divisions to form the vulva.
View Article and Find Full Text PDFJ Aquat Anim Health
December 2024
Virginia Institute of Marine Science, William & Mary, Gloucester Point, Virginia, USA.
Objective: The dinoflagellate Alexandrium monilatum forms blooms during summer in tributaries of the lower Chesapeake Bay. Questions persist about the potential for A. monilatum to negatively affect aquatic organisms.
View Article and Find Full Text PDFJ Clin Invest
December 2024
Immunobiology and Transplant Science Center and Department of Surgery, Houston Methodist Hospital, Texas Medical Center, Houston, United States of America.
T cells have a remarkable capacity to clonally expand, a process that is intricately linked to their effector activities. As vigorously proliferating T cell also incur substantial DNA lesions, how the dividing T cells safeguard their genomic integrity to allow the generation of T effector cells remains largely unknown. Here we report the identification of the apurinic/apyrimidinic endonuclease-1 (Apex1) as an indispensable molecule for the induction of cytopathic T effectors in mouse models.
View Article and Find Full Text PDFGeroscience
December 2024
Division of Solid Organ Transplantation, Department of Surgery, University of Minnesota, 420 Delaware St SE, Minneapolis, MN, 55455, USA.
The proportion of older individuals needing liver transplantation is growing, resulting in an increasingly frail patient population. Frailty constitutes a constellation of cognitive and physical symptoms associated with aging and increases the risk of morbidity and mortality. Senescence is a programmed cell fate in response to stress implicated in causing frailty, age-related diseases, and aging itself.
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