DRhoGEF2, RhoGEF, shar, DRhoGEF, shar pei
induces contractile cell shape changes by stimulating myosin II via the Rho1 pathway - location at the actin cortex regulated by interaction with the microtubule plus-end tracking protein EB1
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.50
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\RhoGEF2 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\RhoGEF2 in GBrowse 2
Maps at 2-80 to 2-85.
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Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
RhoGEF2 activity is required for actin organization and acto-myosin contractility during somatic nuclear divisions, pole cell formation and cellularization of syncytial blastoderm embryos.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Mutations in RhoGEF2 disrupt the coordinates induction of cell shape changes.
RhoGEF2 is essential for the invagination of mesodermal and endodermal primordia during gastrulation.
RhoGEF2 is essential for directing the cell shape changes associated with gastrulation.
Embryos lacking RhoGEF2 (generated as germline clones) show inappropriate lateral folds.
Named "shar pei" after the breed of dog characterized by numerous skin folds, to reflect the phenotype of mutant embryos.