SMG-1 is a phosphatidylinositol kinase-related protein kinase that functions as a key component of the nonsense-mediated RNA decay (NMD) pathway. An allele of
smg-1,
yp3, was isolated from a mortal germline mutant strain that becomes progressively sterile and displays germline tumors at the non-permissive temperature of 25 deg C. However, the progressive sterility phenotype of this strain is a synthetic effect that occurs as a consequence of an additional mutation. Although outcrossed strains homozygous for
smg-1(
yp3), or for the null
smg-1 alleles
r904 and
e1228, do not become progressively sterile, these strains do display a low level of germ cell tumors at 25 deg C. Mammalian SMG proteins function in both NMD as well as the S-phase DNA replication checkpoint. Treatment of C. elegans
smg-1 mutants with hydroxyurea, which perturbs the S-phase checkpoint, can elicit germ cell tumors at the permissive temperature of 20 deg C, mimicking the effect of growth at 25 deg C. We present evidence that
smg-1(
yp3) is a separation-of-function mutation that disrupts the S-phase checkpoint, but not NMD. Thus, the DNA damage signaling function of
smg-1 can suppress germ cell tumors, and the role of
smg-1 in NMD is mechanistically separable from its role in DNA damage signaling.