Disease relevance of Act5C

• The protein also becomes highly enriched in pseudopods, microvilli, axons, denticles, the border cell process, and other membrane projections, potentially by binding to endogenous moesin as well as actin [1].
• Mutations in Myosin ID completely reverse the left-right axis (situs inversus), a phenotype that is dependent on an intact actin cytoskeleton [2].
• We incorporated the Drosophila hsp70 and actin 5C promoters, as well as the hr5 enhancer-driven baculovirus ie1 promoter, into plasmids that allow convenient cloning of heterologous genes into multiple cloning sites [3].
• Intracellular propulsion of Listeria monocytogenes is the best understood form of motility dependent on actin polymerization [4].
• An increase of actin synthesis was also observed during the recovery period after two other stresses: reoxygenation after anoxia and ethanol treatment [5].

Psychiatry related information on Act5C

• Rho GTPase pathways control actin reorganization, while the fragile X mental retardation protein (FMRP) regulates the synthesis of specific proteins [6].

High impact information on Act5C

• However, DmIKK epsilon-mediated degradation of DIAP1 does not regulate apoptosis as might be predicted but instead regulates actin dynamics, cell morphology, and the differentiation of sensory organ precursor cells [7].
• Arthrin formation lags several hours behind that of actin III, implying that ubiquitination coincides with some aspect of myofibril assembly [8].
• This component binds specifically to a 65 bp region of DNA surrounding the start point of transcription of the histone H3, H4, and actin 5C genes [9].
• Two of the genes, act5C and act42A, are expressed in undifferentiated cells and probably encode cytoplasmic actins [10].
• Neuronal filopodia are actin-rich cytoplasmic extensions that are involved in motility and recognition in growth cones and maturing axonal endings [11].

Biological context of Act5C

• We identified P element insertions in the Act5C gene that resulted in a lethal phenotype [12].
• A hybrid transgene containing the protein coding sequence for the Act42A isoform, under the control of the regulatory regions of the Act5C gene, also rescues the lethality of the Act5C mutants [12].
• Tissue patterning must be translated into morphogenesis through cell shape changes mediated by remodeling of the actin cytoskeleton [13].
• The Drosophila p21 activated kinase Mbt regulates the actin cytoskeleton and adherens junctions to control photoreceptor cell morphogenesis [14].
• Constitutive activation of Mbt not only disturbs the actin cytoskeleton but also affects adherens junction organisation indicating a requirement of the protein in cell adhesion dependent processes during photoreceptor cell differentiation [14].

Anatomical context of Act5C

• Actin capping protein {alpha} maintains vestigial-expressing cells within the Drosophila wing disc epithelium [13].
• Imaging Clathrin Dynamics in Drosophila melanogaster Hemocytes Reveals a Role for Actin in Vesicle Fission [15].
• alpha- and beta-Spectrin are major components of a submembrane cytoskeletal network connecting actin filaments to integral plasma membrane proteins [16].
• Localized actin polymerization is required to constrict the apical surface of epithelial cells of the eye imaginal disc to maintain the refined arrangement of the developing ommatidia [17].
• The collective oogenesis defects associated with DRok deficiency reveal its essential role in multiple aspects of proper oocyte formation and suggest that DRok defines a novel class of oogenesis determinants that function as key regulators of several distinct actin-dependent processes required for proper tissue morphogenesis [18].

Associations of Act5C with chemical compounds

• Purification entails lysis in a low salt, sucrose buffer that contains ATP, chromatography on DEAE-cellulose, precipitation with actin in the absence of ATP, gel filtration in a discontinuous KI-KCl buffer system, and hydroxylapatite chromatography [19].
• The cDNA encoding the entire RVGP gene was cloned in an expression plasmid under the control of the constitutive actin promoter (Ac), which was co-transfected into S2 cells together with a hygromycin selection plasmid [20].
• In C6/36 cells, the actin 5C and hr5-ie1 promoters were significantly more active than the hsp70 promoter [3].
• A mutation that changes serine 289 to asparagine almost completely inactivates fascin in vivo; singedS289N mutants have gnarled bristles and are sterile due to a severe defect in nurse cell cytoplasm transport caused by the absence of nurse cell cytoplasmic actin bundles [21].
• Overall, the actin 5C promoter was considerably more effective at driving luciferase expression than either hsp70 or IE1 in cell lines derived from Anopheles, Aedes and Culex species. hsp70 functioned well when induced by heat shock and was also induced to a lesser extent by chemicals such as sodium arsenite [22].

Co-localisations of Act5C

• In mouse fibroblasts, p150-Spir colocalized with F-actin and its overexpression induced clustering of filamentous actin around the nucleus [23].

Regulatory relationships of Act5C

• There was a similar preferential association of topoisomerase II with the 5' ends of transcriptionally repressed actin 5C and 57A genes [24].
• These observations suggest a mechanism by which Abl-mediated signaling networks influence the actin cytoskeleton in neuronal growth cones [25].
• At the postsynapse, aPKC regulates the synaptic cytoskeleton by controlling the extent of Actin-rich and MT-rich areas [26].
• Moreover, Rac1-induced actin remodeling is altered in fibroblasts lacking FMRP or carrying a point-mutation in the KH1 or in the KH2 RNA-binding domain [27].
• However, overexpression of a truncated DroVav mutant (that functions as an oncogene when expressed in NIH3T3 cells) results in striking changes in the actin cytoskeleton, resembling those usually visible following Rac activation [28].
• An increase in F-actin levels induced the dephosphorylation and activation of cofilin via activation of the Ssh phosphatase [29].

Other interactions of Act5C

• Mutations in Sb-sbd are associated with defects in apical cell shape changes critical for the evagination of the leg imaginal disc and with defects in assembly and extension of parallel actin bundles in growing mechanosensory bristles [30].
• Taking advantage of available mutants of Drosophila, we expressed clathrin-EGFP in wasp and shibire mutant backgrounds to study the role of actin and dynamin in CCS dynamics and CME in hemocytes [15].
• In the Drosophila wing, a stripe of Notch activation maintains the dorsal-ventral compartment boundary, through a process that depends on the actin cytoskeleton [31].
• Loss of Shaker currents increased the size of lamellipodia and the number of filopodia, structures associated with the actin cytoskeleton [32].
• Drosophila Spire is an actin nucleation factor [33].

Analytical, diagnostic and therapeutic context of Act5C

• Similarly, in Drosophila, actin and myosin 2 localization and cell constriction at the margin of the epidermis mediate dorsal closure and are controlled by Misshapen [34].
• Actin-myosin structures align across multiple cells during rosette formation, and adherens junction proteins assemble in a stepwise fashion during rosette resolution [35].
• We further show by thin section electron microscopy analysis of mutant and wild-type bristles that the amount of material that connects the actin bundles to the plasma membrane is also limited throughout bristle elongation [36].
• Second, two-dimensional gel electrophoresis was used to examine actin isoforms and whole thorax proteins [37].
• AP-actin binds to skeletal myosin subfragment 1 (S1) and forms a homogeneous complex as demonstrated by analytical ultracentrifugation [38].

References