scholarly journals Subpopulations of vomeronasal sensory neurons with coordinated coexpression of type 2 vomeronasal receptor genes are differentially dependent on Vmn2r1

2018 ◽  
Vol 47 (7) ◽  
pp. 887-900 ◽  
Author(s):  
Sachiko Akiyoshi ◽  
Tomohiro Ishii ◽  
Zhaodai Bai ◽  
Peter Mombaerts

2018 ◽  
Author(s):  
Ryan P Dalton ◽  
G Elif Karagöz ◽  
Jerome Kahiapo ◽  
Ruchira Sharma ◽  
Lisa E Bashkirova ◽  
...  

AbstractMutually-exclusive chemoreceptor expression in olfactory and vomeronasal sensory neurons (OSNs and VSNs) enables odorant discrimination. This configuration involves chemoreceptor mediated activation of the endoplasmic reticulum (ER)-resident kinase PERK. PERK drives translation of the transcription factor ATF5 to preclude additional chemoreceptor expression. ATF5 translation is transient in OSNs but persistent in VSNs, suggesting chemoreceptor-specific modes of PERK activation. Herein, we showed that the ER-lumenal domain (LD) of PERK recognized vomeronasal receptor (VR)-derived peptides, suggesting direct PERK activation drives persistent ATF5 translation in VSNs. In contrast, PERK LD did not recognize olfactory receptor (OR)-derived peptides in vitro, and facilitating OR maturation in vivo prevented PERK activation, suggesting that ORs activate PERK indirectly through a failure to exit the ER. Importantly, impairing or prolonging ATF5 expression drove specific chemoreceptor repertoire biases. Together, these results demonstrate mechanistic divergence in chemoreceptor feedback and establish that differences in PERK activation promote qualitatively different gene regulatory results.



2015 ◽  
Vol 212 (5) ◽  
pp. 2125OIA23
Author(s):  
Asma Amjad ◽  
Andres Hernandez-Clavijo ◽  
Simone Pifferi ◽  
Devendra Kumar Maurya ◽  
Anna Boccaccio ◽  
...  


Nature ◽  
2005 ◽  
Vol 437 (7060) ◽  
pp. 898-901 ◽  
Author(s):  
Hiroko Kimoto ◽  
Sachiko Haga ◽  
Koji Sato ◽  
Kazushige Touhara




2009 ◽  
Vol 12 (12) ◽  
pp. 1551-1558 ◽  
Author(s):  
Trese Leinders-Zufall ◽  
Tomohiro Ishii ◽  
Peter Mombaerts ◽  
Frank Zufall ◽  
Thomas Boehm


Neuroscience ◽  
2014 ◽  
Vol 269 ◽  
pp. 43-58 ◽  
Author(s):  
S. Cherian ◽  
Y. Wai Lam ◽  
I. McDaniels ◽  
M. Struziak ◽  
R.J. Delay


2000 ◽  
Vol 12 (10) ◽  
pp. 3529-3536 ◽  
Author(s):  
Kouhei Inamura ◽  
Makoto Kashiwayanagi


2021 ◽  
Author(s):  
Bradford Hall ◽  
Emma Macdonald ◽  
Margaret Cassidy ◽  
Sijung Yun ◽  
Matthew Sapio ◽  
...  

Pathological sensations caused by peripheral painful neuropathy occurring in Type 2 diabetes mellitus (T2DM) are often described as sharp and burning and are commonly spontaneous in origin. Proposed etiologies implicate dysfunction of nociceptive sensory neurons in dorsal root ganglia (DRG) induced by generation of reactive oxygen species, microvascular defects, and ongoing axonal degeneration and regeneration. To investigate the molecular mechanisms contributing to diabetic pain, DRGs were acquired postmortem from patients who had been experiencing painful diabetic peripheral neuropathy (DPN) and subjected to transcriptome analyses to identify genes contributing to pathological processes and neuropathic pain. DPN occurs in distal extremities resulting in the characteristic glove and stocking pattern. Accordingly, the L4 and L5 DRGs, which contain the perikarya of primary afferent neurons innervating the foot, were analyzed from five DPN patients and compared with seven controls. Transcriptome analyses identified 844 differentially expressed genes. We observed increases in levels of inflammation-associated genes from macrophages in DPN patients that may contribute to increased pain hypersensitivity and, conversely, there were frequent decreases in neuronally-related genes. The elevated inflammatory gene profile and the accompanying downregulation of multiple neuronal genes provide new insights into intraganglionic pathology and mechanisms causing neuropathic pain in DPN patients with T2DM.



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