Sox8, Sox9, and Sox10 constitute subgroup E within the Sox family of transc
ription factors. Many Sox proteins are essential regulators of development.
Sox9, for instance, is required for chondrogenesis and male sex determinat
ion; Soxl0 plays key roles in neural crest development and peripheral gliog
enesis. The function of Sox8 has not been studied so far. Here, we generate
d mice deficient in this third member of subgroup E. In analogy to the case
for the related Sox9 and Sox10, we expected severe developmental defects i
n these mice. Despite strong expression of Sox8 in many tissues, including
neural crest, nervous system, muscle, cartilage, adrenal gland, kidney, and
testis, homozygous mice developed normally in utero, were born at Mendelia
n frequencies, and were viable. A substantial reduction in weight was obser
ved in these mice; however, this reduction was not attributable to signific
ant structural deficits in any of the Sox8-expressing tissues. Because of f
requent coexpression with either Sox9 or Sox10, the mild phenotype of Sox8-
deficient mice might at least in part be due to functional redundancy betwe
en group E Sox proteins.