High impact information on Rac2

• This resistance can be suppressed by reducing the levels of Rho1 or Rac, implicating these GTPases in the behavioral response to ethanol [1].
• A role for Drosophila IAP1-mediated caspase inhibition in Rac-dependent cell migration [2].
• These data define a signaling pathway from Trio to Rac to Pak that links guidance receptors to the growth cone cytoskeleton [3].
• We show that progressive loss of combined Rac1, Rac2 and Mtl activity leads first to defects in axon branching, then guidance, and finally growth [4].
• The guanine nucleotide exchange factor, Trio, is essential for Rac function in axon growth and guidance, but not for epithelial morphogenesis or myoblast fusion [5].

Biological context of Rac2

• Here we analyse the loss-of-function phenotypes of three Rac GTPases in Drosophila mushroom body neurons [4].
• Rac GTPases regulate the actin cytoskeleton to control changes in cell shape [5].
• Here we show a dramatic effect in the context of cellular immunity where, unlike embryonic development, Rac2 appears to have a non-redundant function [6].
• Neutrophil chemotaxis requires Rac activation, yet the Rac activators functioning downstream of chemoattractant receptors remain to be determined [7].
• Amongst them, the EP insertions close to rhomboid, yan and rac2 suggest new roles for these genes in diversification of muscle and/or heart cell lineages [8].

Anatomical context of Rac2

• In DOCK2-deficient neutrophils, chemoattractant-induced activation of both Rac1 and Rac2 were severely impaired, resulting in the loss of polarized accumulation of F-actin and phosphatidylinositol 3,4,5-triphosphate (PIP3) at the leading edge [7].
• Finally, though dominant negative Rac1 is able to block filopodia formation in the overexpression experiments, only Rac2 is necessary for filopodia formed by hemocytes after parasitization [9].
• In both Caenorhabditis elegans and Drosophila, UNC-73/Trio functions in axon guidance by signaling through the Rac GTPase to regulate cytoskeletal rearrangements necessary for growth cone migrations [10].
• Rac promotes epithelial cell rearrangement during tracheal tubulogenesis in Drosophila [11].
• Thus, in the context of Drosophila tracheal development, Rac activity must be maintained at a level necessary to balance the assembly and disassembly of E-Cadherin at cell junctions [11].

Associations of Rac2 with chemical compounds

• Moreover, the innervation of the larval optic neuropil by the 5-HT arborization depends on intact Rac function [12].
• Reorganization of the cytoskeleton, under the control of the guanosine triphosphatase, Rac, is also critical for cell migration [13].

Other interactions of Rac2

• These genes delineate a pathway from Cdc42 and Rac to SCAR and the Arp2/3 complex [14].
• Our analysis of rac2 phenotypes clearly demonstrates that the altered mesodermal level of Rho-GTPase Rac2 can influence specification of a number of cardiac and muscular cell types including those expressing ladybird [8].
• Finding that in rac2 mutants ladybird and even skipped-positive muscle founders are overproduced, indicate a new early function for this gene during segregation of muscle progenitors and/or specification of founder cells [8].

Analytical, diagnostic and therapeutic context of Rac2

• It has been reported that during Drosophila embryonic development, and in cell culture, that the Rac GTPases are redundant [6].

References