Table 1 Execution and timing control defects in PCD lead to the bulged tail phenotype in the grp-1 background.

From: Uridine 5’-monophosphate (UMP) synthesis connects nucleotide metabolism to programmed cell death in C. elegans

Genotype

% animals with a bulged tail

Wild-type

0%

grp-1(gm350)

6%

Defects in execution of cell death result in an aberrant bulged tail

egl-1(n1084n3082)

2%

grp-1(gm350); egl-1(n1084n3082)

87%

ced-9(n1950)

5%

grp-1(gm350) ced-9(n1950)

94%

ced-4(n1162)

8%

ced-4(n1162) grp-1(gm350)

94%

ced-3(n717)

1%

grp-1(gm350); ced-3(n717)

86%

ced-3(n2427)

0%

grp-1(gm350); ced-3(n2427)

92%

ced-3(n2923)

1%

grp-1(gm350); ced-3(n2923)

43%

Defects in timing control of cell death result in an aberrant bulged tail

ced-8(n1891)

0%

grp-1(gm350); ced-8(n1891)

80%

Defects in engulfment do not cause an aberrant bulged tail

ced-1(e1735)

0%

ced-1(e1735); grp-1(gm350)

8%

ced-12(bz187)

1%

ced-12(bz187); grp-1(gm350)

8%

Defects in DNA degradation do not cause an aberrant bulged tail

cps-6(ok1718)

0%

cps-6(ok1718); grp-1(gm350)

8%

cnt-1(tm2313)

1%

cnt-1(tm2313); grp-1(gm350)

12%

  1. The percentages of animals displaying a bulged tail phenotype were assessed at the L3-L4 stages using a dissecting microscope for the indicated genotypes (n = 300 from three independent experiments).