scholarly journals The transcription factor Phox2b distinguishes between oral and non-oral sensory neurons in the geniculate ganglion

2017 ◽  
Vol 525 (18) ◽  
pp. 3935-3950 ◽  
Author(s):  
Lisa Ohman-Gault ◽  
Tao Huang ◽  
Robin Krimm
Keyword(s):  
Transcription Factor ◽  
Sensory Neurons ◽  
Geniculate Ganglion ◽  
Oral Sensory

scholarly journals Cell non-autonomous requirement of p75 in the development of geniculate oral sensory neurons

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tao Tang ◽  
Christopher R. Donnelly ◽  
Amol A. Shah ◽  
Robert M. Bradley ◽  
Charlotte M. Mistretta ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Significant Loss ◽  
Taste Buds ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Tactile Stimuli ◽  
Oral Sensory ◽  
Nerve Recordings

AbstractDuring development of the peripheral taste system, oral sensory neurons of the geniculate ganglion project via the chorda tympani nerve to innervate taste buds in fungiform papillae. Germline deletion of the p75 neurotrophin receptor causes dramatic axon guidance and branching deficits, leading to a loss of geniculate neurons. To determine whether the developmental functions of p75 in geniculate neurons are cell autonomous, we deleted p75 specifically in Phox2b + oral sensory neurons (Phox2b-Cre; p75fx/fx) or in neural crest-derived cells (P0-Cre; p75fx/fx) and examined geniculate neuron development. In germline p75−/− mice half of all geniculate neurons were lost. The proportion of Phox2b + neurons, as compared to Phox2b-pinna-projecting neurons, was not altered, indicating that both populations were affected similarly. Chorda tympani nerve recordings demonstrated that p75−/− mice exhibit profound deficits in responses to taste and tactile stimuli. In contrast to p75−/− mice, there was no loss of geniculate neurons in either Phox2b-Cre; p75fx/fx or P0-Cre; p75fx/fx mice. Electrophysiological analyses demonstrated that Phox2b-Cre; p75fx/fx mice had normal taste and oral tactile responses. There was a modest but significant loss of fungiform taste buds in Phox2b-Cre; p75fx/fx mice, although there was not a loss of chemosensory innervation of the remaining fungiform taste buds. Overall, these data suggest that the developmental functions of p75 are largely cell non-autonomous and require p75 expression in other cell types of the chorda tympani circuit.

scholarly journals Transcription factor ATF5 is required for terminal differentiation and survival of olfactory sensory neurons

2012 ◽  
Vol 109 (45) ◽  
pp. 18589-18594 ◽  
Author(s):  
S.-Z. Wang ◽  
J. Ou ◽  
L. J. Zhu ◽  
M. R. Green
Keyword(s):  
Transcription Factor ◽  
Sensory Neurons ◽  
Terminal Differentiation ◽  
Olfactory Sensory Neurons

MafA transcription factor identifies the early ret-expressing sensory neurons

2010 ◽  
pp. NA-NA ◽  
Author(s):  
Laure Lecoin ◽  
Nathalie Rocques ◽  
Warif El-Yakoubi ◽  
Sarrah Ben Achour ◽  
Magalie Larcher ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Sensory Neurons

REGULATION OF TRANSCRIPTION FACTOR C-JUN BY NERVE GROWTH FACTOR IN ADULT SENSORY NEURONS

1993 ◽  
Vol 52 (3) ◽  
pp. 309
Author(s):  
B. G. Gold ◽  
T. Storm-Dickerman ◽  
W. C. Mobley ◽  
D. R. Austin
Keyword(s):  
Transcription Factor ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Sensory Neurons ◽  
Regulation Of Transcription ◽  
Nerve Growth ◽  
Factor C

scholarly journals Targeted molecular profiling of rare olfactory sensory neurons identifies fate, wiring, and functional determinants

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
J Roman Arguello ◽  
Liliane Abuin ◽  
Jan Armida ◽  
Kaan Mika ◽  
Phing Chian Chai ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase Ii ◽  
Sensory Neurons ◽  
Chromatin Accessibility ◽  
Olfactory Sensory Neurons ◽  
Ionotropic Receptor ◽  
Genetic Switch ◽  
Pou Domain ◽  
Guidance Molecule ◽  
Neuronal Guidance

Determining the molecular properties of neurons is essential to understand their development, function and evolution. Using Targeted DamID (TaDa), we characterize RNA polymerase II occupancy and chromatin accessibility in selectedIonotropic receptor(Ir)-expressing olfactory sensory neurons inDrosophila. Although individual populations represent a minute fraction of cells, TaDa is sufficiently sensitive and specific to identify the expected receptor genes. UniqueIrexpression is not consistently associated with differences in chromatin accessibility, but rather to distinct transcription factor profiles. Genes that are heterogeneously expressed across populations are enriched for neurodevelopmental factors, and we identify functions for the POU-domain protein Pdm3 as a genetic switch of Ir neuron fate, and the atypical cadherin Flamingo in segregation of neurons into discrete glomeruli. Together this study reveals the effectiveness of TaDa in profiling rare neural populations, identifies new roles for a transcription factor and a neuronal guidance molecule, and provides valuable datasets for future exploration.

scholarly journals Olfactory and Vomeronasal Receptor Feedback Employ Divergent Mechanisms of PERK Activation

2018 ◽  
Author(s):  
Ryan P Dalton ◽  
G Elif Karagöz ◽  
Jerome Kahiapo ◽  
Ruchira Sharma ◽  
Lisa E Bashkirova ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Transcription Factor ◽  
Sensory Neurons ◽  
Olfactory Receptor ◽  
Vomeronasal Receptor ◽  
Gene Regulatory ◽  
Lumenal Domain ◽  
Vomeronasal Sensory Neurons

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.

scholarly journals microRNA-dependent control of sensory neuron function regulates posture behaviour in Drosophila

2020 ◽  
Author(s):  
M. Klann ◽  
A.R. Issa ◽  
C.R. Alonso
Keyword(s):  
Transcription Factor ◽  
Sensory Neurons ◽  
Competitive Inhibition ◽  
Sensory Function ◽  
Bhlh Transcription Factor ◽  
Systematic Analysis ◽  
Evolutionarily Conserved ◽  
Morphological Defects ◽  
Behavioural Tests ◽  
Null Mutants

ABSTRACTAll what we see, touch, hear, taste or smell must first be detected by the sensory elements in our nervous system. Sensory neurons, therefore, represent a critical component in all neural circuits and their correct function is essential for the generation of behaviour and adaptation to the environment. Here we report that a gene encoding the evolutionarily conserved microRNA (miRNA) miR-263b, plays a key behavioural role in Drosophila through effects on the function of larval sensory neurons. Several independent experiments support this finding. First, miRNA expression analysis by means of a miR-263b reporter line, and fluorescent-activated cell sorting coupled to quantitative PCR, both demonstrate expression of miR-263b in Drosophila larval sensory neurons. Second, behavioural tests in miR-263b null mutants show defects in self-righting: an innate and evolutionarily conserved posture control behaviour that allows the larva to return to its normal position if turned upside-down. Third, competitive inhibition of miR-263b in sensory neurons using a miR-263b ‘sponge’ leads to self-righting defects. Fourth, systematic analysis of sensory neurons in miR-263b mutants shows no detectable morphological defects in their stereotypic pattern. Fifth, genetically-encoded calcium sensors expressed in the sensory domain reveal a reduction in neural activity in miR-263b null mutants. Sixth, miR-263b null mutants show a reduced ‘touch-response’ behaviour and a compromised response to sound, both characteristic of larval sensory deficits. Furthermore, bioinformatic miRNA target analysis, gene expression assays, and behavioural phenocopy experiments suggest that miR-263b might exert its effects – at least in part – through repression of the bHLH transcription factor atonal. Altogether, our study suggests a model in which miRNA-dependent control of transcription factor expression affects sensory function and behaviour. Building on the evolutionary conservation of miR-263b, we propose that similar processes may modulate sensory function in other animals, including mammals.

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