[C.elegansII] e404 : sluggish, poor backing, dumpyish; somewhat Egl; multiple defects in neuronal outgrowth, branching; also defects in excretory canal extension, gonad arm growth; males have abnormal bursal anatomy. ES2 ME0. OA>5: n152, n166, n569 (synergizes with sem-5(n177) to give strong Sem migration defect),e2432, e2499, etc. Null phenotype uncertain; some lethality in strong alleles. Cloned: multiple transcripts (different 5' ends); one encodes 1528 aa protein, predicted to bind actin, ATP/GTP; may interact with SEM-5. Transgene overexpression leads to extension of growth cones along a-p axis. [Hedgecock et al. 1987; Hekimi and Kershaw 1993; UG]
unc-53 encodes at least five large (~1200-1600 residue) proteins, orthologous to human NAV1, NAV2/RAINB1 (OMIM:607026), and NAV3, and homologous to Drosophila CG10662; UNC-53 proteins are required for anteroposterior guidance of migrating cells, axons, and excretory cell canals; unc-53 mutations affect egg laying, backward locomotion, body size, and male mating; UNC-53 proteins vary in their N-terminal regions but share common C-terminal sequences with a AAA-ATPase domain; the UNC-53 N-terminus physically interacts with ABI-1, suggesting that UNC-53 may function as a scaffold to link the ARP2/3 complex to ABI-1; UNC-53 also interacts both physically and genetically with SEM-5; unc-53 is expressed in those cells requiring it, suggesting that its function is cell-autonomous; overexpression of unc-53 induces excess cellular outgrowth.
Predicted to enable actin filament binding activity. Involved in several processes, including backward locomotion; positive regulation of locomotion; and reproductive behavior. Located in cytoplasm. Expressed in several structures, including excretory cell; hermaphrodite distal tip cell; neurons; non-striated muscle; and socket cell. Is an ortholog of human NAV1 (neuron navigator 1).