The role of Arabidopsis S6 Kinase 1 (AtS6K1), a downstream target of TOR kinase, in controlling plant growth and ribosome biogenesis was characterized after generating transgenic plants expressing AtS6K1 under auxin-inducible promoter. Down regulation of selected cell cycle regulatory genes upon auxin treatment was observed in the transgenic plants, confirming the negative regulatory role of AtS6K1 in the plant cell cycle progression reported earlier. Callus tissues established from these transgenic plants grew to larger cell masses with more number of enlarged cells than untransformed control, demonstrating functional implication of AtS6K1 in the control of plant cell size. The observed negative correlation between the expression of AtS6K1 and the cell cycle regulatory genes, however, was completely reversed in protoplasts generated from the transgenic plants expressing AtS6K1, suggesting a possible existence of dual regulatory mechanism of the plant cell cycle regulation mediated by AtS6K1. An alternative method of kinase assay, termed "substrate-mediated kinase pull down", was employed to examine the additional phosphorylation on other domains of AtS6K1 and verified the phosphorylation of both amino- and carboxy-terminal domains, which is a novel finding regarding the phosphorylation target sites on plant S6Ks by upstream regulatory kinases. In addition, this kinase assay under the stress conditions revealed the salt- and sugar-dependencies of AtS6K1 phosphorylations.
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http://dx.doi.org/10.1007/s10059-012-2275-4 | DOI Listing |
Cell Rep
January 2025
Molecular Immunology, Justus-Liebig-University Giessen, 35392 Giessen, Germany. Electronic address:
Control of cell proliferation is critical for the lymphocyte life cycle. However, little is known about how stage-specific alterations in cell cycle behavior drive proliferation dynamics during T cell development. Here, we employed in vivo dual-nucleoside pulse labeling combined with the determination of DNA replication over time as well as fluorescent ubiquitination-based cell cycle indicator mice to establish a quantitative high-resolution map of cell cycle kinetics of thymocytes.
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January 2025
Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
Neurogenic microRNAs 9/9 and 124 (miR-9/9-124) drive the direct reprogramming of human fibroblasts into neurons with the initiation of the fate erasure of fibroblasts. However, whether the miR-9/9-124 fate erasure logic extends to the neuronal conversion of other somatic cell types remains unknown. Here, we uncover that miR-9/9-124 induces neuronal conversion of multiple cell types: dura fibroblasts, astrocytes, smooth muscle cells, and pericytes.
View Article and Find Full Text PDFFEBS J
January 2025
Université d'Angers, Inserm, CNRS, CRCI2NA, ICO, Angers, France.
Senescence is a tumor suppressor mechanism triggered by oncogene expression and chemotherapy treatment. It orchestrates a definitive cessation of cell proliferation through the activation of the p53-p21 and p16-Rb pathways, coupled with the compaction of proliferative genes within heterochromatin regions. Some cancer cells have the ability to elude this proliferative arrest but the signaling pathways involved in circumventing senescence remain to be characterized.
View Article and Find Full Text PDFMol Microbiol
January 2025
Laboratório de Biologia Molecular de Patógenos (LBMP), Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo (Unifesp), São Paulo, Brazil.
Leishmania presents a complex life cycle that involves both invertebrate and vertebrate hosts. By regulating gene expression, protein synthesis, and metabolism, the parasite can adapt to various environmental conditions. This regulation occurs mainly at the post-transcriptional level and may involve epitranscriptomic modifications of RNAs.
View Article and Find Full Text PDFNPJ Precis Oncol
January 2025
Zentalis Pharmaceuticals, Inc., San Diego, CA, USA.
Upregulation of Cyclin E1 and subsequent activation of CDK2 accelerates cell cycle progression from G1 to S phase and is a common oncogenic driver in gynecological malignancies. WEE1 kinase counteracts the effects of Cyclin E1/CDK2 activation by regulating multiple cell cycle checkpoints. Here we characterized the relationship between Cyclin E1/CDK2 activation and sensitivity to the selective WEE1 inhibitor azenosertib.
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