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Table 3 Dauer and aging genes regulated by TGFβ signaling.

From: Regulation of signaling genes by TGFβ during entry into dauer diapause in C. elegans

Gene Induces or represses dauer?a Fold regulationb p value
insulin pathway
   daf-2 (receptor) strongly represses -3.1 <0.0001
   akt-2 represses -3.0 <0.0001
   akt-1 allc represses 1.0 ns
   akt-1ac unknown -1.8 <0.003
   akt-1bc unknown 1.4 <0.03
   pdk-1 represses 1.8 <0.0001
   daf-16ad unknown 1.0 ns
   daf-16 alld promotes -1.7 <0.0004
Insulin-like ligands
   ins-4 repressese -2.1 <0.002
   ins-5 unknown -2.6 <0.02
   ins-6 repressese -2.6 <0.02
   ins-7 represses -2.1 <0.005
   ins-18 promotese 1.8 <0.002
   ins-33 unknown 3.9 <0.0003
   ins-35 unknown 6.5 <0.0001
insulin receptor-like
   F56A4.C unknown -3.5 <0.0001
   Y19D10A.7 unknown -2.8 <0.0003
   F14D2.6 unknown 1.8 <0.006
   F15E11.11 unknown 1.8 <0.008
other dauer and aging regulators
   daf-12 strongly induces 2.2 <0.0007
   daf-5 induces -2.0 <0.0003
   daf-9 represses -4.2 <0.02
   scl-1 unknown 5.2 <0.006
  1. ns, not significant This
  2. table shows all insulin-like ligands, insulin-receptor-like genes, TGFβ, and insulin/IGF pathway genes with greater than 1.8-fold regulation and a p value less than 0.05. Genes checked for regulation that showed <1.8 fold regulation or p > 0.05 or both: clk-1, clk-2, sir-2.1, daf-11, daf-7, daf-1, daf-4, daf-14, daf-8, daf-3, daf-19, tax-4, npc-1, daf-18, age-1, old-1, mev-1, hsf-1, daf-21, gpa-2, gpa-3, kin-29, kin-8, unc-3 and tph-1, as well as all genes annotated as insulins present on the microarray (ins-2, ins-3, ins-11, ins-17, ins-22, ins-23, ins-24, ins-26, ins-30, ins-32, ins-34, ins-37) and nearly all genes identified as putative insulin receptors in Dlakic [27].
  3. aInduction or repression of dauer is defined by mutant or RNAi loss-of-function phenotypes unless otherwise noted. daf-9 mutants have characteristics similar to both types, and are thus marked "mixed".
  4. cThe fold change between mutant dauers and wild-type. A positive number indicates higher expression in dauers, a negative number indicates higher expression in N2.
  5. cThe table entry "akt-1 all" is for a probe that recognizes both isoforms. The other two akt-1 entries each cover an exon unique to the indicated isoform.
  6. dThe entry "daf-16a isoform" is for a probe that recognizes:R13H8.1c (daf-16a1), R13H8.1b (daf-16a2), and R13H8.1d, but not R13H8.1a (daf-16b) or R13H8.1e. The entry "daf-16 all" is for a probe that recognizes all five isoforms of daf-16.
  7. eOverexpression of ins-4 or ins-6 represses dauer in a daf-28 mutant [7]. ins-6 has also been shown biochemically to act as a receptor agonist [25]. Overexpression of ins-18 promotes dauer [24].