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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].
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BMC Developmental Biology

ISSN: 1471-213X

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