Swainrubin3341

© 2020. Published by The Company of Biologists Ltd.Stressed cells downregulate translation initiation and assemble membrane-less foci termed stress granules (SGs). Extensively characterized in cultured cells, the existence of such structures in stressed adult stem cell pools remain poorly characterized. Here we report that Drosophila orthologs of mammalian SG components AGO1, ATX2, CAPRIN, eIF4E, FMRP, G3BP, LIN-28, PABP, and TIAR are enriched in adult intestinal progenitor cells where they accumulate in small cytoplasmic messenger ribonucleoprotein complexes (mRNPs). Treatment with sodium arsenite or rapamycin reorganized these mRNPs into large cytoplasmic granules. Formation of these intestinal progenitor stress granules (IPSGs) depended on polysome disassembly, led to translational downregulation, and was reversible. While canonical SG nucleators ATX2 and G3BP were sufficient for IPSG formation in the absence of stress, neither of them, nor TIAR, either individually or collectively, were required for stress-induced IPSG formation. This work therefore finds that IPSGs do not assemble via a canonical mechanism, raising the possibility that other stem cell populations employ a similar stress-response mechanism. Solcitinib concentration © 2020. Published by The Company of Biologists Ltd.Cell shape morphogenesis from spherical to polygonal occurs in epithelial cell formation in metazoan embryogenesis. In syncytial Drosophila embryos, the plasma membrane incompletely surrounds each nucleus and is organized as a polygonal epithelial-like array. Each cortical syncytial division cycle shows circular to polygonal plasma membrane transition along with furrow extension between adjacent nuclei from interphase to metaphase. In this study, we assess the relative contribution of DE-cadherin and Myosin II at the furrow for polygonal shape transition. We show that polygonality initiates during each cortical syncytial division cycle when the furrow extends from 4.75 to 5.75 µm. Polygon plasma membrane organization correlates with increased junctional tension, increased DE-cadherin and decreased Myosin II mobility. DE-cadherin regulates furrow length and polygonality. Decreased Myosin II activity allows for polygonality to occur at a lower length than controls. Increased Myosin II activity leads to loss of lateral furrow formation and complete disruption of polygonal shape transition. Our studies show that DE-cadherin-Myosin II balance regulates an optimal lateral membrane length during each syncytial cycle for polygonal shape transition. © 2020. Published by The Company of Biologists Ltd.Abiotic and biotic factors cause plant wounding and trigger complex short- and long-term responses at the local and systemic levels. These responses are under the control of complex signaling pathways, which are still poorly understood. Here, we show that the rapid activation of clade-A Mitogen Activated Protein Kinases (MAPKs) MPK3 and MPK6 by wounding depends on the upstream MAPK Kinases (MAP2Ks) MKK4 and MKK5 but is independent of jasmonic acid (JA) signaling. In addition, this fast module does not control wound-triggered JA accumulation in Arabidopsis, unlike its orthologues in tobacco. We also demonstrate that a second MAPK module, composed of MKK3 and the clade-C MAPKs MPK½/7, is activated by wounding in a MKK4/5-independent manner. We provide evidence that the activation of this MKK3-MPK½/7 module occurs mainly through wound-induced JA production via the transcriptional regulation of upstream clade-III MAP3Ks, particularly MAP3K14. We show that mkk3 mutant plants are more susceptible to herbivory from larvae of the generalist lepidopteran herbivore Spodoptera littoralis, indicating that the MKK3-MPK½/7 module is involved in counteracting insect feeding. © 2020 American Society of Plant Biologists. All rights reserved.Spatiotemporal regulation of gene expression is critical for proper developmental timing in plants and animals. The transcription factor FUSCA3 (FUS3) regulates developmental phase transitions by acting as a link between hormonal pathways in Arabidopsis thaliana. However, the mechanisms governing its spatiotemporal expression pattern are poorly understood. Here, we show that FUS3 is repressed in the ovule integuments and seed endosperm. FUS3 repression requires class I BASIC PENTACYSTEINE (BPC) proteins, which directly bind GA/CT cis-elements in FUS3 and restrict its expression pattern. During vegetative and reproductive development, FUS3 derepression in bpc1-1 bpc2 (bpc½) double mutant or misexpression in ProML1FUS3 lines causes dwarf plants carrying defective flowers and aborted ovules. Postfertilization, ectopic FUS3 expression in bpc½ endosperm or ProML1FUS3 endosperm and endothelium increases endosperm nuclei proliferation and seed size, causing delayed or arrested embryo development. These phenotypes are rescued in bpc½ fus3-3. Lastly, class I BPCs interact with FIS-PRC2 (FERTILIZATION-INDEPENDENT SEED-Polycomb Repressive Complex2), which represses FUS3 in the endosperm during early seed development. We propose that BPC1 and 2 promote the transition from reproductive to seed development by repressing FUS3 in ovule integuments. After fertilization, BPC1 and 2 and FIS-PRC2 repress FUS3 in the endosperm to coordinate early endosperm and embryo growth. © 2020 American Society of Plant Biologists. All rights reserved.The antagonistic regulation of seed germination by the phytohormone ABA and GA has been well-established. However, how these phytohormones antagonistically regulate root growth and branching (tillering in rice) remains obscure. Rice Tiller Enhancer (TE) encodes an activator of the APC/CTE E3 ubiquitin ligase complex that represses tillering but promotes seed germination. In this study, we found a dual role of GA and APC/CTE in regulating root growth. High GA levels can activate APC/CTE to promote the degradation of OsSHR1 (a key promoting factor of root growth) in the root meristem (RM) or MOC1 (a key promoting factor of tillering) in the axillary meristem (AM), leading to restricted root growth and tillering; while low GA levels can activate the role of APC/CTE in stimulating RM cell division to promote root growth. In addition, we found that moderate enhancement of ABA signaling helps to maintain the RM or AM size to sustain root growth or tillering by antagonizing GA-promoted degradation of OsSHR1 and MOC1 through the SnRK2-APC/CTE regulatory module.