Zinc finger protein sall2 is not essential for embryonic and kidney development.
SALL/Sall is a mammalian homolog of the Drosophila region-specific homeotic gene spalt (sal), and heterozygous mutations in SALL1 in humans lead to Townes-Brocks syndrome. We earlier reported that mice deficient in Sall1 die in the perinatal period and that kidney agenesis or severe dysgenesis are present. We have now generated mice lacking Sall2, another Sall family gene. Although Sall2 is expressed mostly in an overlapping fashion versus that of Sall1, Sall2-deficient mice show no apparent abnormal phenotypes. Morphology and gene expression patterns of the mutant kidney were not affected. Mice lacking both Sall1 and Sall2 show kidney phenotypes comparable to those of Sall1 knockout, thereby demonstrating the dispensable roles of Sall2 in embryonic and kidney development.
Sato
Akira
A
Division of Stem Cell Regulation, The Institute of Medical Science, The University of Tokyo, Japan.
Matsumoto
Yuko
Y
Koide
Urara
U
Kataoka
Yuki
Y
Yoshida
Nobuaki
N
Yokota
Takashi
T
Asashima
Makoto
M
Nishinakamura
Ryuichi
R
D000818:Animals; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D007668:Kidney / Q000196:embryology* / Q000473:pathology / Q000502:physiology*; D051379:Mice; D008817:Mice, Mutant Strains; D051762:PAX2 Transcription Factor; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism*; D016335:Zinc Fingers
D004268:DNA-Binding Proteins; D051762:PAX2 Transcription Factor; C497319:Pax2 protein, mouse; C104147:SALL2 protein, human; C491254:Sall1 protein, mouse; D014157:Transcription Factors