Cpd-1 null mice display a subtle neurological phenotype.
BACKGROUND
CPD1 (also known as ANP32-E) belongs to a family of evolutionarily conserved acidic proteins with leucine rich repeats implicated in a variety of cellular processes regulating gene expression, vesicular trafficking, intracellular signaling and apoptosis. Because of its spatiotemporal expression pattern, CPD1 has been proposed to play an important role in brain morphogenesis and synaptic development.


RESULTS
We have generated CPD1 knock-out mice that we have subsequently characterized. These mice are viable and fertile. However, they display a subtle neurological clasping phenotype and mild motor deficits.


CONCLUSIONS
CPD1 is not essential for normal development; however, it appears to play a role in the regulation of fine motor functions. The minimal phenotype suggests compensatory biological mechanisms.
Kular
Rupinder K
RK
Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
Gogliotti
Rocky G
RG
Opal
Puneet
P
D000818:Animals; D002460:Cell Line; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018832:Molecular Chaperones; D009043:Motor Activity; D009419:Nerve Tissue Proteins / Q000172:deficiency* / Q000235:genetics*; D009422:Nervous System Diseases / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D010641:Phenotype; D012098:Reproduction
C435730:Anp32e protein, mouse; D018832:Molecular Chaperones; D009419:Nerve Tissue Proteins