Chromosomal localisation of the mouse and human peripherin genes

Moncla, Anne; Landon, Françoise; Matteï, Marie‐Geneviève; Portier, Marie‐Madeleine

doi:10.1017/s0016672300030330

Cited by 16 publications

(11 citation statements)

References 36 publications

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“…1983/84). It is classified in the type III IF family based on its gene structure and on the coding sequence homologous to vimentin, GFAP and desmin (Thompson and Ziff 1989; Moncla et al . 1992).…”

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Reduced number of unmyelinated sensory axons in peripherin null mice

Larivière¹,

Nguyen

Ribeiro‐da‐Silva³

et al. 2002

Journal of Neurochemistry

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Peripherin is a type III intermediate filament (IF) abundantly expressed in developing neurons, but in the adult, it is primarily found in neurons extending to the peripheral nervous system. It has been suggested that peripherin may play a role in axonal elongation and/or cytoskeletal stabilization during development and regeneration. To further clarify the function of peripherin, we generated and characterized mice with a targeted disruption of the peripherin gene. The peripherin null mice were viable, reproduced normally and did not exhibit overt phenotypes. Microscopic analysis revealed no gross morphological defects in the ventral and dorsal roots, spinal cord, retina and gut, but protein analyses showed increased levels of the type IV IF a-internexin in ventral roots of peripherin null mice. Whereas the number and caliber of myelinated motor and sensory axons in the L5 roots remained unchanged in peripherin knockout mice, there was a substantial reduction ( 34%) in the number of L5 unmyelinated sensory fibers that correlated with a decreased binding of the lectin IB4. These results demonstrate a requirement of peripherin for the proper development of a subset of sensory neurons. Keywords: CGRP, dorsal root ganglion neurons, IB4, intermediate filament, sensory and motor neuronstransgenic mice.

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“…Peripherin was first discovered as being the major IF protein in neuroblastoma cell lines and in rat pheochromocytoma cells (PC12; Portier et al 1983/84). It is classified in the type III IF family based on its gene structure and on the coding sequence homologous to vimentin, GFAP and desmin (Thompson and Ziff 1989;Moncla et al 1992).…”

mentioning

confidence: 99%

Reduced number of unmyelinated sensory axons in peripherin null mice

Larivière¹,

Nguyen

Ribeiro‐da‐Silva³

et al. 2002

Journal of Neurochemistry

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“…The Clipr-59 probe was designed by PCR to precisely encompass the deleted region of CLIPR-59 cDNA in KO mice (nucleotides 374-889 in cDNA). The peripherin probe was kindly provided by M. M. Portier (Moncla et al, 1992). Cell counts was performed at E18.5, as described previously (Backer et al, 2007).…”

Section: In Situ Hybridization and Mn Countsmentioning

confidence: 99%

CLIPR-59: a protein essential for neuromuscular junction stability during mouse late embryonic development

et al. 2013

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CLIPR-59 is a new member of the cytoplasmic linker proteins (CLIP) family mainly localized to the trans-Golgi network. We show here that Clipr-59 expression in mice is restricted to specific pools of neurons, in particular motoneurons (MNs), and progressively increases from embryonic day 12.5 (E12.5) until the first postnatal days. We generated a Clipr-59 knockout mouse model that presents perinatal lethality due to respiratory defects. Physiological experiments revealed that this altered innervation prevents the normal nerve-elicited contraction of the mutant diaphragm that is reduced both in amplitude and fatigue-resistance at E18.5, despite unaffected functional muscular contractility. Innervation of the mutant diaphragm is not altered until E15.5, but is then partially lost in the most distal parts of the muscle. Ultrastructural observations of neuromuscular junctions (NMJs) in the distal region of the diaphragm reveal a normal organization, but a lower density of nerve terminals capped by terminal Schwann cells in E18.5 mutant when compared with control embryos. Similar defects in NMJ stability, with a hierarchy of severity along the caudo-rostral axis, are also observed in other muscles innervated by facial and spinal MNs in Clipr-59 mutant mice. Clipr-59 deficiency therefore affects axon maintenance but not axon guidance toward muscle targets. Thus, CLIPR-59 is involved in the stabilization of specific motor axons at the NMJ during mouse late embryogenesis and its role is crucial for mouse perinatal development.

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“…We recently identified mutations in the voltage gated sodium channel, Scn8a, that is encoded by the med locus Kohrman et al 1996a,b). In the course of evaluating candidate genes for med, we refined the map positions of four genes that were previously assigned to this region either by in situ hybridization or by lowresolution genetic mapping: contactin (Cntn1; Gennarini et al 1989), peripherin (Prph; Pendleton et al 1991;Moncla et al 1992), the calcium channel beta subunit 3 (Cchb3; Chin et al 1995), and natural resistance-associated macrophage protein 2 (Nramp2; Gruenheid et al 1995).…”

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confidence: 99%

“…The close linkage of these neuron-specific genes suggests that they might be regulated by shared cis-acting elements. These three genes, along with Nramp 2, Cntn1, and the Hoxc cluster, have been mapped to a conserved linkage group of human Chr 12q11-12q13 Collin et al 1994;Moncla et al 1992;Vidal et al 1995;Berglund and Ranscht 1994). We have determined the gene order for six mouse loci in this linkage group, but the arrangement of the human genes has not been determined.…”

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confidence: 99%