Transcription regulatory networks in Caenorhabditis elegans

aat-5 encodes a predicted amino acid transporter catalytic subunit; unlike catalytic subunits in other organisms, however, AAT-5 does not contain the highly conserved cysteine residue known to facilitate covalent interaction with a glycoprotein subunit, suggesting that AAT-5 does not require this residue for heterodimer formation or alternatively, does not require the glycoprotein subunit for function.

abl-1 encodes, by alternative splicing, three isoforms of a Src homology (SH) 2 and 3 domain-containing non-receptor tyrosine kinase orthologous to human ABL1 (OMIM:189980, mutated in chronic myeloid leukemia) and ABL2 (OMIM:164690); ABL-1 inhibits germline apoptosis induced by radiation or by natural aging, but it has no effect on apoptosis induced by starvation or by chemical mutagens (ethylnitrosourea, ethylmethanesulfonate, cisplatin, etoposide), or on constitutive ('physiological') germline apoptosis; at the same time, ABL-1 is required for germline apoptosis induced by oxidative, osmotic or heat-shock stress, and is also required for pathogenesis by Shigella flexneri infecting the intestine; ABL-1-inhibited apoptosis is confined to a single gonad arm undergoing radiation, having no nonautonomous effect on the unirradiated arm; abl-1 is expressed in the germline, in most or all cells of early embryos, and in postembryonic pharynx, tail ganglia and ventral nerve cord; abl-1(ok171) mutants are hypersensitive to germline apoptosis and resistant to S. flexneri infection; both abl-1(ok171) phenotypes are phenocopied by c-ABL inhibitors such as STI-571 (Gleevec); ABL-1-inhibited apoptosis requires active CED-3 and EGL-1, inactive CED-9, and active AKT-1, CEP-1, CLK-1, HUS-1, and MRT-2; abl-1(ok171) has no effect on somatic apoptosis, and abl-1(ok171) mutants are generally normal; abl-1 transcripts are enriched in cultured unc-4::GFP neurons.

abt-5 encodes a predicted ATP-binding cassette (ABC) transporter that is a member of the ABCA subfamily of transport proteins; ABT-5 is predicted to function as a transmembrane protein that couples energy to transport of various molecules across membranes, but as loss of abt-5 activity via RNAi results in no obvious defects, the precise role of abt-5 in C. elegans development and/or behavior is not yet known; abt-5 promoter-gfp fusion proteins are expressed in larvae and adults in the intestine and in unidentified cells in the head.

ace-3 encodes one of four C. elegans acetylcholinesterases (AChE); ACE-3 represents ~5% of the total AChE activity in C. elegans and in vitro, hydrolyzes acetylthio-, butyrylthio-, and propionylthiocholine substrates with equal efficiency; although loss-of-function mutations in ace-3 result in no obvious defects, animals doubly mutant with ace-1 or ace-2 have slight defects in backward locomotion and animals triply mutant for ace-1, -2, and -3 arrest as unhatched, yet fully developed, embryos; ace-3 is the downstream gene in an operon with a fourth AChE-encoding gene, ace-4, and transcriptional reporter fusions with ace-4 upstream sequences direct expression in pharyngeal muscles pm3, 4, 5, and 7, the two CAN (canal associated neuron) cells, midbody dorsal body wall muscles in larvae, and several neurons in the head and anal ganglion

aco-1 encodes an aconitase that is homologous to mammalian iron regulatory protein-1 (IRP1); aco-1 activity is required for normal brood sizes and, under iron stress conditions, for normal lifespan and L4-to-adult growth rates; ACO-1 physically interacts with GEX-3; like IRP1, ACO-1 has aconitase activity and is post-translationally regulated by iron, but, unlike IRP1, it lacks RNA-binding activity; ACO-1 is predicted to be mitochondrial, and its mRNA levels appear to decrease in response to iron treatment.

A homolog of an alpha type nicotinic acetylcholine receptor subunit involved in the mediation of fast synaptic transmission at neuromuscular junctions.

A homolog of an alpha type nicotinic acetylcholine receptor subunit involved in the mediation of fast synaptic transmission at neuromuscular junctions.

act-3 encodes an invertebrate actin, highly similar to ACT-1, ACT-2, and ACT-4, that functions in body wall muscle; act-3 functions with two other action isoforms, act-1 and act-2, to control cytoplasmic microfilament function in the early embryo.

acy-2 encodes an adenylyl cyclase; an intragenic deletion of acy-2 is lethal at the first larval stage of development; the terminal phenotype resembles that seen in loss-of-function gsa-1 mutants.

ads-1 encodes an ortholog of human ALKYL-DIHYDROXYACETONEPHOSPHATE SYNTHASE PRECURSOR (AGPS; OMIM:603051) that is required for normal larval development; mutation of human AGPS leads to type 3 rhizomelic chondrodysplasia punctata (OMIM:600121).