Acts as a transcription factor during mitochondrial stress by activating the mitochondrial unfolded protein response (mtUPR) (PubMed:22700657, PubMed:25274306, PubMed:25773600, PubMed:30642431). Induces nuclear and mitochondrial gene transcription, including genes coding for mitochondrial chaperones and proteins involved in glycolysis, amino acid catabolism and innate immunity (PubMed:22700657, PubMed:25274306, PubMed:25773600). Following mitochondrial stress, restores mitochondrial respiratory capacity by limiting the transcription of oxidative phosphorylation (OXPHOS) machinery genes and by promoting the assembly of OXPHOS complexes via the up-regulation of chaperone and assembly factor genes (PubMed:25773600). Component of a feedback loop involving atfs-1, atgl-1 and hlh-11 (PubMed:33078707). Acts together with flp-7 to negatively regulate the expression of the transcription regulator hlh-11, to promote expression of atgl-1, and thus atgl-1-dependent fat oxidation in response to mitochondrial stress (PubMed:33078707). In addition, functions with hlh-11 to maintain lifespan (PubMed:33078707). Promotes mtDNA maintenance and propagation of deleterious mtDNA (PubMed:27135930). In absence of mitochondrial stress, localizes mainly to mitochondria where it is rapidly degraded by protease lonp-1 (PubMed:22700657). Upon mitochondrial stress which causes a reduction in protein mitochondrial import, accumulates in the cytoplasm and translocates into the nucleus to activate transcription of mitochondrial unfolded protein response genes (PubMed:22700657). Similarly, accumulates in the nucleus in response to P.aeruginosa-mediated infection (PubMed:25274306). Ubiquitously expressed. Induced by mitochondrial stress. May be desumoylated by ulp-4. Prevents the up-regulation of several innate immune genes following P.aeruginosa-mediated infection (PubMed:25274306). RNAi-mediated knockdown causes a reduction in survival following P.aeruginosa-mediated infection (PubMed:25274306). Prevents the up-regulation of mitochondrial protective genes and increases the transcription of oxidative phosphorylation machinery and tricarboxylic acid cycle genes following mitochondrial stress caused by RNAi-mediated knockdown of protease spg-7 (PubMed:22700657, PubMed:25773600). Assembly of complex I and ATP synthase of the oxidative phosphorylation machinery and oxygen consumption are reduced in a spg-7 RNAi-mediated background (PubMed:25773600). RNAi-mediated knockdown reduces the levels of deleterious mtDNA that occurs in aging cells (PubMed:27135930). Protection from death following anoxia-reperfusion is lost in a spg-7 RNAi-mediated background (PubMed:27459203). RNAi-mediated knockdown does not alter atgl-1 expression (PubMed:33078707). However, RNAi-mediated knockdown increases atgl-1 expression in a hlh-11 ok2944 mutant background (PubMed:33078707). RNAi-mediated knockdown reduces the induction of hsp-60, an indicator of mitochondrial stress following overexpression of flp-7 (PubMed:33078707). Belongs to the bZIP family.