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Biology subjects

de Jesus, B. N.

Publications and source records attributed to de Jesus, B. N..

3 recordsLinked to original sources

Chromosomes remain individualized through interphase in embryos of the tardigrade Hypsibius exemplaris

Tardigrades are microscopic animals that can survive exceptional levels of ionizing radiation or desiccation - DNA-damaging conditions that would kill most animals. Irradiation or radiomimetic drug treatment of the tardigrade Hypsibius exemplaris can induce remarkably high expression levels of DNA repair genes, primarily those in the base excision repair and nonhomologous end joining pathways. How tardigrades can repair widespread DNA damage without producing frequent, large-scale chromosome structural abnormalities, like chromosome translocations and fusions, is unknown. Here, we report the results of examining chromosome and nuclear architecture throughout the cell cycle in early embryos of H. exemplaris. We found that H. exemplaris chromosomes are maintained in an individualized form throughout the cell cycle. We were surprised to also find that each chromosome is housed in a fully or partially separate lamin-lined compartment, instead of all chromosomes being housed in a single, nearly spherical nuclear lamina and envelope. Our results reveal unusual chromosomal and nuclear organization in a tardigrade. We speculate that these unexpected features might limit chromosomal rearrangements during DNA damage repair in extreme conditions. SIGNIFICANCE STATEMENTO_LIWe have investigated unusual chromosome organization in an organism that survives extremely DNA-damaging environments, a tardigrade, through early embryonic cell cycles. C_LIO_LIChromosomes in fixed and stained embryos appeared more condensed through interphase than is typical for animal cells. C_LIO_LIChromosomes remained individualized, in fully or partially separate lamin-lined compartments, through interphase. C_LIO_LIThe results reveal a unique nuclear and chromosomal organization in tardigrades, which we speculate might contribute to limiting chromosomal structure abnormalities under DNA damaging conditions in nature. C_LI

cell biology↗

Opposing actomyosin pools generate cortical flows that establish epithelial polarity

Epithelial cell polarity, defined by distinct apical and basolateral domains, is fundamental for animal embryonic development and organ function. During organogenesis, epithelia often develop from unpolarized precursor cells. How mammalian epithelial cells establish polarity de novo from an initially unpolarized state has remained unclear, in part due to an inability to observe this process in real time in non-transformed cellular systems. Here, we leverage recent advances in 3D spheroid culture of mouse embryonic stem cells, fluorescent protein knock-in and live imaging techniques to study the process of epithelial polarity establishment. We show that apical myosin activity, regulated by Myosin Light Chain Kinase (MLCK), is crucial for the establishment and maintenance of epithelial polarity. Actomyosin cortical flows transport ZO-1, a tight junction component that interacts with apical polarity proteins, to establish the apical membrane. A second pool of myosin, regulated by Rho kinase, localizes basally and balances apically directed flow. Our result imply that epithelial polarity emerges as a consequence of actomyosin-driven cytoskeletal rearrangements.

cell biology↗

Temporally distinct roles of Aurora A in polarization of the C. elegans zygote

During asymmetric cell division, coordination of cell polarity and the cell cycle is critical for proper inheritance of cell fate determinants and generation of cellular diversity. In Caenorhabditis elegans (C. elegans), polarity is established in the zygote and is governed by evolutionarily conserved Partitioning defective (PAR) proteins that localize to distinct cortical domains. At the time of polarity establishment, anterior and posterior PARs segregate to opposing cortical domains that specify asymmetric cell fates. Timely establishment of these PAR domains requires a cell cycle kinase, Aurora A (AIR-1 in C.elegans). Aurora A depletion by RNAi causes a spectrum of phenotypes including no posterior domain, reversed polarity, and excess posterior domains. How depletion of a single kinase can cause seemingly opposite phenotypes remains obscure. Using an auxin-inducible degradation system, drug treatments, and high-resolution microscopy, we found that AIR-1 regulates polarity via distinct mechanisms at different times of the cell cycle. During meiosis I, AIR-1 acts to prevent the formation of bipolar domains, while in meiosis II, AIR-1 is necessary to recruit PAR-2 onto the membrane. Together these data clarify the origin of the multiple polarization phenotypes observed in RNAi experiments and reveal multiple roles of AIR-1 in coordinating PAR protein localization with the progression of the cell cycle.

developmental biology↗