Academic Thesis

Basic information

Name Katayama Keiichi
Belonging department
Occupation name
researchmap researcher code B000305947
researchmap agency Okayama University of Science

Title

Deletion of Sema3a or plexinA1/plexinA3 Causes Defects in Sensory Afferent Projections of Statoacoustic Ganglion Neurons

Bibliography Type

 

Author

Kei-ichi Katayama
Fumiyasu Imai
Fumikazu Suto
Yutaka Yoshida

Summary

Statoacoustic ganglion (SAG) neurons project sensory afferents to appropriate targets in the inner ear to form functional vestibular and auditory circuits. Neuropilin1 (Npn1), a receptor for class 3 semaphorins, is required to generate appropriate afferent projections in SAG neurons
 however, the ligands and coreceptors involved in Npn1 functioning remain unknown. Here we show that both plexinA1 and plexinA3 are expressed by SAG neurons, and plexinA1/plexinA3 double mutant mice show defects in afferent projections of SAG neurons in the inner ear. In control mice, sensory afferents of SAG neurons terminate at the vestibular sensory patches, whereas in plexinA1/plexinA3 double mutants, they extend more dorsally in the inner ear beyond normal vestibular target areas. Moreover, we find that semaphorin3a (Sema3a) is expressed in the dorsal otocyst, and Sema3a mutant mice show defects in afferent projections of SAG neurons similar to those observed in plexinA1/plexinA3 double mutants and in mice lacking a functional Npn1 receptor. Taken together, these genetic findings demonstrate that Sema3a repellent signaling plays a role in the establishment of proper afferent projections in SAG neurons, and this signaling likely occurs through a receptor complex involving Npn1 and either plexinA1 or plexinA3. © 2013 Katayama et al.

Magazine(name)

PLoS ONE

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Volume

8

Number Of Pages

8

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Date of Issue

2013-08-26

Referee

Exist

Invited

Not exist

Language

English

Thesis Type

Research papers (academic journals)

ISSN

 

DOI

10.1371/journal.pone.0072512

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PMID

 

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