Dauer arrest and longevity in C. elegans are controlled by an insulin-like pathway containing
daf-2 , an insulin receptor-like gene, and
age-1 , a
p110-like subunit of PI(3)K. To identify cells where this pathway functions, transgenic animals with cell-type restricted
age-1 expression were constructed by expressing an
age-1 cDNA from tissue-specific promoters: in neurons from the pan-neuronal
unc-14 promoter; in mechanosensory (plus a few other) neurons from the
mec-7 promoter; in muscle from the
unc-54 promoter; in the intestine using a gut-specific synthetic promoter (Marshall, S. and J. McGhee, in prep). Transgenic animals with extrachromosomal arrays of the promoter-cDNA fusions were examined for the ability of cell-type restricted
age-1 expression to rescue the dauer-constitutive, aging and metabolic phenotypes of
age-1(
mg44) . Dauer arrest was rescued by
age-1 expression in any of the above tissues, showing that
age-1 action in a variety of different cells is sufficient, but not necessary, for non-dauer development. These results suggest that
age-1 regulates a hormonal output from any of several sources for non-dauer development, as suggested by the genetic mosaic analysis of
daf-2 (Apfeld, J. and C. Kenyon, 1998). The extended lifespan of
age-1(
mg44) was only rescued by pan-neuronal
age-1 expression. In agreement, pan-neuronal expression of a
daf-2 cDNA rescued the extended lifespan of
daf-2(
e1370) . Expression of
age-1 from the
mec-7 , muscle, or gut promoters was unable to restore normal lifespan to
age-1(
mg44) . These results suggest that control of aging may be limited to the nervous system. The metabolic effects of
age-1 also appear to be controlled in a specific subset of cells. Sudan Black staining of
age-1(
mg44) reveals enhanced fat accumulation in the intestine. Muscle
age-1 expression was able to rescue the fat accumulation defects of
age-1(
mg44) , while this phenotype was not rescued by
age-1 expression in any other tissues. We conclude that dauer formation, longevity and metabolism are controlled cell non-autonomously by
age-1 , but that these
age-1 outputs are controlled independently in different cell types.