Disease relevance of Act57B

• Mutations in Myosin ID completely reverse the left-right axis (situs inversus), a phenotype that is dependent on an intact actin cytoskeleton [1].
• Here, wild-type (WT) human alpha-cardiac actin and a mutant E99K actin have been expressed and purified from the baculovirus/insect cell expression system [2].

High impact information on Act57B

• 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 [3].
• 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 [4].
• ERM proteins regulate cell morphology and plasma membrane dynamics by reversibly anchoring actin filaments to integral plasma membrane proteins [5].
• In Drosophila rhabdomeres, NINAC interacts with actin filaments and with a PDZ scaffolding protein to organize the phototransduction machinery into a signaling complex [6].
• Recombinant DNA clones that contained sea urchin genomic DNA fragments were constructed and screened for the presence of actin-encoding DNA sequences by colony hybridization with the Drosophila actin sequence [7].

Biological context of Act57B

• Act57B transcription is first detected in visceral muscle precursors and is detectable in all embryonic muscles by the end of embryogenesis [8].
• To identify regulatory events occurring during myogenesis, we characterized the transcriptional regulation of a Drosophila melanogaster actin gene, Actin 57B [8].
• Here we have addressed how two actin regulators, capping protein, a barbed end binding protein, and the Arp2/3 complex, a potent actin assembly nucleator, function to generate properly organized bundles [9].
• 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 [10].
• These defects are associated with abnormalities in DRok-dependent actin dynamics and appear to be mediated by multiple downstream effectors of activated DRok that have previously been implicated in oogenesis [10].

Anatomical context of Act57B

• Recent studies have identified key Src64-dependent mechanisms that regulate actin cytoskeletal dynamics during the growth of actin-rich ring canals, which act as intercellular bridges between germ cells [11].
• Myosin VI stabilizes an actin network during Drosophila spermatid individualization [12].
• Drosophila melanogaster bristle development is dependent on actin assembly, and prominent actin bundles form against the elongating cell membrane, giving the adult bristle its characteristic grooved pattern [9].
• In fibroblasts, Shroom readily associates with actin stress fibers and induces bundling, Apxl is found on cortical actin, and KIAA1202 is localized to a cytoplasmic population of F-actin [13].
• In salivary glands and follicle cells the head and neck domains were concentrated in the cell nucleus, where the minus end of each actin filament is located [14].

Associations of Act57B with chemical compounds

• 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 [15].

Other interactions of Act57B

• Moreover, many cardioblasts express increased levels of muscle-specific genes such as myosin, actin 57B, and Mlp60A, a protein that is restricted to the somatic, visceral, and pharyngeal muscles [16].

Analytical, diagnostic and therapeutic context of Act57B

• Using quantitative polymerase chain reaction, we determined that expression of the MEF2-regulated actin gene Act57B was severely reduced in these animals [17].
• 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 [18].
• Actin-myosin structures align across multiple cells during rosette formation, and adherens junction proteins assemble in a stepwise fashion during rosette resolution [19].
• Organization of actin gene sequences in the sea urchin: molecular cloning of an intron-containing DNA sequence coding for a cytoplasmic actin [7].
• Southern blot hybridization experiments with both the Drosophila actin sequence and one of the cloned sea urchin sequences, in conjunction with solution hybridization data, suggest an actin gene copy number of 5-20 per haploid genome [7].

References