Syntaxin 1A is required for normal in utero development.
We have generated a syntaxin 1A knockout mouse by deletion of exons 3 through 6 and a concomitant insertion of a stop codon in exon 2. Heterozygous knockout animals were viable with no apparent phenotype. In contrast, the vast majority of homozygous animals died in utero, with embryos examined at day E15 showing a drastic reduction in body size and development when compared to WT and heterozygous littermates. Surprisingly, out of a total of 204 offspring from heterozygous breeding pairs only four homozygous animals were born alive and viable. These animals exhibited reduced body weight, but showed only mild behavioral deficiencies. Taken together, our data indicate that syntaxin 1A is an important regulator of normal in utero development, but may not be essential for normal brain function later in life.
McRory
John E
JE
Department of Physiology and Biophysics, The Hotchkiss Brain Institute, University of Calgary, 3330 Hospital Dr. NW, Calgary, Canada T2N 4N1.
Rehak
Renata
R
Simms
Brett
B
Doering
Clinton J
CJ
Chen
Lina
L
Hermosilla
Tamara
T
Duke
Carlie
C
Dyck
Richard
R
Zamponi
Gerald W
GW
D000818:Animals; D018388:Codon, Terminator / Q000235:genetics; D047108:Embryonic Development / Q000235:genetics; D005091:Exons / Q000235:genetics; D005260:Female; D005313:Fetal Death / Q000235:genetics; D020567:Fetal Weight / Q000235:genetics; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D051381:Rats; D017384:Sequence Deletion; D050827:Syntaxin 1 / Q000235:genetics / Q000502:physiology*; D014599:Uterus / Q000502:physiology*
D018388:Codon, Terminator; C494214:Stx1a protein, mouse; D050827:Syntaxin 1