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Complex phenotype of mice homozygous for a null mutation in the Sp4 transcription factor gene
Author(s) -
Göllner Heike,
Bouwman Peter,
Mangold Monika,
Karis Alar,
Braun Harald,
Rohner Iris,
Del Rey Adriana,
Besedovsky HugoOskar,
Meinhardt Andreas,
Van Den Broek Marion,
Cutforth Tyler,
Grosveld Frank,
Philipsen Sjaak,
Suske Guntram
Publication year - 2001
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1046/j.1365-2443.2001.00455.x
Subject(s) - biology , transcription factor , gene , exon , phenotype , zinc finger , genetics , transcription (linguistics) , knockout mouse , null allele , zinc finger transcription factor , microbiology and biotechnology , linguistics , philosophy
Background Sp4 is a zinc finger transcription factor which is closely related to Sp1 and Sp3. All three proteins recognize the same DNA elements and can act as transcriptional activators through glutamine‐rich activation domains. Unlike Sp1 and Sp3, which are ubiquitous proteins, Sp4 is highly abundant in the central nervous system, but also detectable in many other tissues. Results We have disrupted the mouse Sp4 gene by a targeted deletion of the exons encoding the N‐terminal activation domains. Sp4 knockout mice show a complete absence of Sp4 expression. They develop until birth without obvious abnormalities. After birth, two‐thirds die within 4 weeks. Surviving mice are growth retarded. Male Sp4 null mice do not breed. The cause for the breeding defect remains obscure since they show complete spermatogenesis. In addition, pheromone receptor genes in the vomeronasal organ appear unaffected. Female Sp4 null mice have a smaller thymus, spleen and uterus. In addition, they exhibit a pronounced delay in sexual maturation. Conclusions The phenotype of the Sp4 null mice differs significantly from those described for Sp1 –/– and Sp3 –/– mice. Thus, the structural similarities, the common recognition motif and the overlapping expression pattern of these three transcription factors do not reflect similar physiological functions.