5/31/2023 0 Comments Drosophila germline clone xAlthough both HOW(L) and HOW(S) can bind the same mRNA target, they act in opposing directions binding of HOW(L) to stripe mRNA at the 3′ UTR leads to mRNA degradation, whereas the binding of HOW(S) leads to the stabilization of stripe mRNA( Nabel-Rosen et al., 2002). The how gene is differentially spliced into two isoforms, HOW(L) and HOW(S), which share the same signature of the RNA-binding domain but differ at their C-terminal region. In the Drosophila embryo, HOW regulates heart-beat rate, mesoderm invagination, muscle-dependent tendon cell differentiation and glial maturation ( Baehrecke, 1997 Nabel-Rosen et al., 1999 Zaffran et al., 1997). elegans ( Crittenden et al.,2002 Crittenden et al.,2003 Hansen and Schedl,2006), and the maturation of Schwann cells in the PNS and oligodendrocytes in the CNS mediated by QKI in mammalian species( Ebersole et al., 1996 Hardy, 1998 Larocque and Richard, 2005). The STAR RBPs are essential for the control of transitional differentiation states - including the transition from mitosis to meiosis and sex-determination mediated by GLD-1 in C. HOW belongs to the STAR(signal transduction and activation of RNA) family( Vernet and Artzt, 1997),which includes the Caenorhabditis elegans homolog GLD-1, and the mammalian quaking (QKI, QK) protein. The RNA-binding protein (RBP) Held out wing (HOW) is highly expressed in the mesoderm during early embryogenesis. Regulation of RNA metabolism is essential for a variety of developmental processes. In summary, our analysis suggests that HOW downregulates the levels of a number of mRNA species in the mesoderm in order to enable proper mesoderm spreading during early embryogenesis. In addition, the number of EVE-positive cells, which are responsive to receptor tyrosine kinase (RTK) signaling, was increased following Miple overexpression in the mesoderm and appeared to be dependent on Heartless function. Further analysis showed that overexpressing one of these genes, miple (a Drosophila midkine and pleiotrophin heparin-binding growth factor), in the mesoderm led to abnormal scattered MAPK activation, a phenotype that might explain the abnormal mesoderm spreading. Importantly, overexpression of three of these genes phenocopied the mesoderm-spreading phenotype of howgermline clone embryos. Four mRNAs were found to be specifically elevated in the mesoderm of how germline clone embryos, and to exhibit specific binding to HOW via their 3′ UTRs. To identify direct HOW targets, we implemented a series of selection methods on mRNAs whose levels were elevated in how germline clone embryos during the stage of mesoderm spreading. HOW is an RNA-binding protein that is thought to regulate diverse mRNA targets. In how germline clone embryos, defects in mesoderm spreading lead to a partial loss of dorsal mesoderm derivatives. The even spreading of mesoderm cells in the Drosophila embryo is essential for its proper patterning by ectodermally derived signals.
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