Transcriptional activator that binds to the consensus sequence 5'-[AT]GATA[AG]-3' (PubMed:7782329, PubMed:15733671, PubMed:18003741, PubMed:18024960, PubMed:18448117, PubMed:26700680, PubMed:26016853, PubMed:26963674). Predominantly directs the transcription of intestinal genes such as ges-1, cpr-6, pho-1, ftn-1, vit-2 and lev-11, and itself (PubMed:9659934, PubMed:10518545, PubMed:15733671, PubMed:18448117, PubMed:19111532, PubMed:26700680, PubMed:26963674). Required for gut-specific differentiation, specifically acting with the GATA region-binding transcription factor elt-7 to control normal gene expression and promote normal formation of the intestine (PubMed:20807527). Regulates intestinal gene expression in response to hypoxia to promote longevity (PubMed:25284791). Modulation of longevity may, in part, be the result of regulation of expression of daf-16 isoforms d and f in the intestine (PubMed:24834345). Regulates tissue specific gene expression at basal levels and in response to bacterial infection in the intestine to control innate immunity (PubMed:16968778, PubMed:21168435, PubMed:25340560, PubMed:26016853). Plays a role in the induction of metal-responsive genes, activating gene expression from zinc-activated promoters and iron-dependent promoters and enhancers (PubMed:18024960, PubMed:22194696, PubMed:25552416). May regulate the expression of genes that control sensitivity to oxidative stress, in a mab-3-dependent manner, and osmotic stress, in conjunction with the GATA region-binding transcription factor elt-3 (PubMed:17901115, PubMed:20498281, PubMed:20126308). May play a role in sphingolipid signaling by regulating the expression of the sphingosine-1-phosphate degrading enzyme, sphingosine-1-phosphate lyase (PubMed:15734735). May act with the Notch signaling pathway to promote endodermal gene expression (PubMed:18003741). Has a protective role in response to infection by Gram-negative bacteria such as S.enterica, E.coli, P.aeruginosa and B.pseudomallei, Gram-positive bacterium E.faecalis and fungal pathogen C.neoformans (PubMed:16968778, PubMed:17183709, PubMed:21168435, PubMed:23980181, PubMed:30265660). An association with the 26S proteasome regulatory subunit rpt-6, in part, controls gene expression in response to infection by P.aeruginosa (PubMed:30265660). Regulates gene expression during the recovery phase following a bacterial infection (PubMed:25340560, PubMed:30265660). May act with p38-activated transcription factors to control p38 gene induction in response to bacterial infection (PubMed:22967128, PubMed:26016853). Controls lysosome formation in the intestine by controlling lysosomal gene expression (PubMed:26828939). Interacts with lag-1 (PubMed:18003741). Interacts with pha-4 (PubMed:18448117). Interacts with rpt-6 (PubMed:30265660). Expressed in discrete foci within nuclei of the gut in embryos. Expressed in the intestine. Expressed at all stages but more highly during embryogenesis, with expression beginning at the 2E cell stage (endodermal stage). Expression continues to adulthood. By P.aeruginosa infection. May be ubiquitinated in response to infection by B.pseudomallei. Animals do not survive for long beyond hatching and frequently die at the L1 larval stage (PubMed:9659934, PubMed:20807527). Upon attempts to feed, food accumulates behind the pharynx and there is blockage of the brush border that surrounds the gut lumen in surviving L1 stage larvae (PubMed:9659934, PubMed:20807527). RNAi-mediated knockdown results in a reduced body size and reduced gene expression from zinc-activated promoters and of genes related to the immune response (PubMed:25552416, PubMed:26016853). This reduction in target gene expression is enhanced when infected with B. pseudomallei (PubMed:23980181). RNAi-mediated knockdown results in increased sensitivity and mortality when exposed to Gram-negative bacteria such as S.enterica, E.coli, P.aeruginosa and B.pseudomallei, Gram-positive bacterium E.faecalis and fungal pathogen C.neoformans (PubMed:16968778, PubMed:17183709, PubMed:21168435, PubMed:23980181, PubMed:30265660). Furthermore, when exposed to E.coli and P.aeruginosa, the intestines distend due to the colonization and proliferation of its bacterial content (PubMed:16968778, PubMed:17183709, PubMed:21168435). RNAi-mediated knockdown at the L4 larval stage, in addition, prevents the recovery of P.aeruginosa infected animals treated with the antibiotic streptomycin (PubMed:30265660). RNAi-mediated knockdown also results in increased sensitivity to heat and to arsenite- and paraquat-induced oxidative stress (PubMed:16968778, PubMed:20498281). RNAi-mediated knockdown results in fewer intestinal lysosomes (PubMed:26828939). RNAi-mediated knockdown during larval development results in smaller animals (PubMed:26016853). RNAi-mediated knockdown specifically during the L4 larval stage inhibits the expression of intestinal genes such as gsto-1, which is normally induced under hypoxic conditions, prevents increased longevity induced by transient hypoxia exposure and prevents mitohormesis when exposed to the mitochondrial reactive oxygen species-generating agent paraquat (PubMed:25284791). In addition, RNAi-mediated knockdown at this stage prevents the expression of genes that are usually up-regulated during recovery in response to tetracycline or kanamycin treatment following an infection and furthermore, prevents the recovery of S. enterica infected animals treated with tetracycline (PubMed:25340560). RNAi-mediated knockdown on an elt-3 knockout background results in increased sensitivity to osmotic stress (PubMed:20126308). Double mutation with elt-7 results in arrest at the L1 stage of larval development, reduced expression of gut-specific genes and a severe disruption to normal gut differentiation with the absence of birefringent and rhabditin granules, which are characteristic of normal gut differentiation, largely at the regions of the cell that interface with the pharyngeal and rectal valves (PubMed:20807527). These mutants also have essentially no gut lumen, with the infrequent occurance of patches of lumen and brush border in few animals, and reduced gut epithelialization as indicated by reduced expression of epithelial markers erm-1b, itx-1 and ajm-1 (PubMed:20807527). RNAi-mediated knockdown specifically during the L4 larval stage reduces the expression of daf-16 isoforms d and f, but has little or effect on isoform a.