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Table 4 Rescue of AVKR pathfinding defects

From: Analysis of C. elegans NR2E nuclear receptors defines three conserved clades and ligand-independent functions

TRANSGENE

GENOTYPE

% AVKR DEFECT

N

p

none

wild-type

0

27

 

none

fax-1 (gm83)

78

32

 

fax-1 9 kb genomic DNA

fax-1 (gm83)

12

25

 

none

fax-1 (gm83) lin-15 (n765)

97

35

 

FAX-1::INV FAX-1

fax-1 (gm83) lin-15 (n765)

92

53

0.55

FAX-1::FAX-1 LBD

fax-1 (gm83) lin-15 (n765)

33

52

<0.001

FAX-1::CbFAX-1 LBD

fax-1 (gm83) lin-15 (n765)

36

22

<0.001

FAX-1::NHR-111 LBD

fax-1 (gm83) lin-15 (n765)

61

95

<0.001

FAX-1::NHR-67 LBD

fax-1 (gm83) lin-15 (n765)

41

39

<0.001

FAX-1::Δ LBD

fax-1 (gm83) lin-15 (n765)

62

63

<0.001

  1. The percentage of the AVKR axon crossover defect [56] is shown for each strain. N = number of AVKR axons examined. p = Chi square P values relative to fax-1(gm83) lin-15(n756) strain without any transgene.