The major gene for neural tube defects, ct, in the curly-tail (CT) mou
se strain was mapped previously to mouse chromosome 4 by combining lin
kage data from several backcrosses. The penetrance of the neural tube
trait, already incomplete in the CT strain, was further reduced in sev
eral of these backcrosses, suggesting the existence of recessive modif
iers or strain-specific susceptibility alleles. Here we describe the m
apping of a curly-tail modifier locus, mct1, to chromosome 17 in moder
ate and low penetrance crosses of CT with BALB/cByJ and Mus spretus. N
o effect of mct1 was seen in a higher penetrance cross with the BXD-8/
Ty strain, confirming that ct is the major gene in the model. Homozygo
sity at both ct and mct1 loci was sufficient to account for all of the
affected individuals in the BALB/cByJ cross and most of the affected
individuals in the M. spretus cross and was the preferred model overal
l. No evidence was found for epistatic interaction between ct and mct1
. (C) 1995 Academic Press, Inc.