Expression pattern of Anosmin‐1 during pre‐ and postnatal rat brain development

Abstract

Anosmin-1 participates in the development of the olfactory and GnRH systems. Defects in this protein are responsible for both the anosmia and the hypogonadotrophic hypogonadism found in Kallmann's syndrome patients. Sporadically, these patients also manifest some neurological symptoms that are not explained in terms of the developmental defects in the olfactory system. We describe the pattern of Anosmin-1 expression in the central nervous system during rat development using a novel antibody raised against Anosmin-1 (Anos1). The areas with Anos1-stained neurons and glial cells were classified into three groups: (1) areas with immunoreactivity from embryonic day 16 to postnatal day (P) 15; (2) areas with Anosmin-1 expression only at postnatal development; (3) nuclei with immunoreactivity only at P15. Our data show that Anos1 immunoreactivity is detected in projecting neurons and interneurons within areas of the brain that may be affected in patients with Kallmann's syndrome that develop both the principal as well as sporadic symptoms. Developmental Dynamics 237:2518 -2528, 2008.

Anosmin-1a is required for fasciculation and terminal targeting of olfactory sensory neuron axons in the zebrafish olfactory system

“…The distribution of anosmin-1a in the brain of zebrafish embryos did not match precisely with earlier investigations of the distribution of KAL-1 mRNA and/or anosmin-1 in chick, human, rat and musk shrew embryos (Legouis et al, 1993;Rugarli et al, 1993;Soussi-Yanicostas et al, 1996;Hardelin et al, 1999;Dellovade et al, 2003;Clemente et al, 2008). In particular, investigations performed on human foetuses aged from 4 to 10 weeks of gestation demonstrated a strong accumulation of the protein in OB from 5 week of gestation onward and a complete absence of anosmin-1 expressing cells in the OE (Hardelin et al, 1999).…”

FGF-2 and Anosmin-1 Are Selectively Expressed in Different Types of Multiple Sclerosis Lesions

“…During optic nerve development, Anosmin-1 is expressed by OPCs and optic axons, and inactivation of this protein reduces their adhesiveness to different substrates, including Anosmin-1 . Indeed, Anosmin-1 is misexpressed in the X-linked Kallmann syndrome, wherein some alterations in myelinated commissures and tracts containing numerous Anosmin-1 ϩ oligodendrocytes have been described Mayston et al, 1997;Farmer et al, 2004;Clemente et al, 2008). Thus, these data point to Anosmin-1 as a potentially important factor in oligodendroglial biology during the onset of MS.…”

Lateralization of motor control in the human nervous system: genetics of mirror movements

“…The presence of a bilateral CST in these patients was first supported by TMS results [74], with recent MRI approaches confirming abnormalities in the CST but also cortical structures such as the corpus callosum and internal capsule [72,75]. Interestingly, anosmin-1, the protein product of KAL-1, is expressed by oligodendrocytes in the CST and corpus callosum [76], suggesting that it indirectly affects development of neurons through its effect on glial cells. The role of the other Kallmann syndrome genes FGFR1 and PROK2/PROKR2 in MM awaits further study.…”