Kallmann syndrome: adhesion, afferents, and anosmia.
Three new studies into the function of human anosmin-1 and related proteins in C. elegans and rodents show that these influence axon branching and axon targeting. The rodent anosmin appears to work at two stages of development, initially promoting axon outgrowth from the olfactory bulb and then stimulating branching from axons into the olfactory cortex. CeKal-1 further influences morphogenesis, and, as the human and nematode anosmins are functionally conserved, these studies provide insights into the pathogenesis of Kallmann syndrome (KS).
MacColl
Gavin
G
Neuroendocrine Unit, Department of Medicine, Royal Free and University College Medical School, Royal Free Campus, Rowland Hill Street, London NW3 2PF, United Kingdom.
Bouloux
Pierre
P
Quinton
Richard
R
D000818:Animals; D002448:Cell Adhesion / Q000235:genetics; D015815:Cell Adhesion Molecules / Q000172:deficiency / Q000235:genetics; D002454:Cell Differentiation / Q000235:genetics*; D002465:Cell Movement / Q000235:genetics*; D016326:Extracellular Matrix Proteins; D006801:Humans; D017436:Kallmann Syndrome / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D009419:Nerve Tissue Proteins / Q000172:deficiency / Q000235:genetics; D000857:Olfaction Disorders / Q000235:genetics*; D009833:Olfactory Pathways / Q000002:abnormalities* / Q000378:metabolism / Q000503:physiopathology
C076266:ANOS1 protein, human; D015815:Cell Adhesion Molecules; D016326:Extracellular Matrix Proteins; D009419:Nerve Tissue Proteins