| 175175 | Q9TZC4 | ILKH_CAEEL | Integrin-linked protein kinase homolog pat-4 (ILK homolog) (Paralyzed and arrested elongation at two-fold protein 4) | DISRUPTION PHENOTYPE | Embryonic lethality due to 1.5 fold stage-onset paralysis. Mutant embryos have defects in maintaining polarization of several components involved in the assembly of dense bodies and M lines, such as integrin pat-3, unc-89 and unc-112 to muscle attachment sites (PubMed:12015115). RNAi-mediated knockdown causes sterility resulting from oocyte accumulation in the proximal gonad and distal tip cell (DTC) migration defects (33 percent of animals). Actin cytoskeleton in the proximal gonad appears disorganized (PubMed:16476426). RNAi-mediated knockdown results in impaired mobility, mitochondrial fragmentation and disrupted integrin attachment complexes in muscle (PubMed:22253611). This leads to degradation of muscle proteins in the cytosol, myofibrillar defects and disruption of sarcomere organization (PubMed:22253611). RNAi-mediated knockdown in hatched embryos but not in adults causes adult-onset paralysis characterized by the collapse of myosin filaments in body wall muscles and a decrease in pharyngeal pumping (PubMed:24314125). In L1 larval stage, results in the formation of large myosin aggregates in body wall muscle cells (PubMed:22761445). In L4 larval stage, causes ectopic membrane extensions from body wall muscles (PubMed:16495308). In adults, causes an increase in lifespan, resistance to heat stress and increased expression of stress response factors hsf-1, sod-3, hsp-16.2 and gst-4 (PubMed:24314125). {ECO:0000269|PubMed:12015115, ECO:0000269|PubMed:16476426, ECO:0000269|PubMed:16495308, ECO:0000269|PubMed:22253611, ECO:0000269|PubMed:22761445, ECO:0000269|PubMed:24314125}. |