Drosophila Mechanosensory Transduction

2020 ◽  
Author(s):  
Philip Hehlert ◽  
Wei Zhang ◽  
Martin C. Göpfert
Keyword(s):  
Mechanosensory Transduction

scholarly journals Distinct roles for innexin gap junctions and hemichannels in mechanosensation

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Denise S Walker ◽  
William R Schafer
Keyword(s):  
Blood Pressure ◽  
Heterologous Expression ◽  
Pain Perception ◽  
Mechanosensory Transduction ◽  
Wide Range ◽  
Touch Receptor Neurons ◽  
Touch Sensitivity ◽  
Range Of Functions ◽  
Receptor Neurons ◽  
And Control

Mechanosensation is central to a wide range of functions, including tactile and pain perception, hearing, proprioception, and control of blood pressure, but identifying the molecules underlying mechanotransduction has proved challenging. In Caenorhabditis elegans, the avoidance response to gentle body touch is mediated by six touch receptor neurons (TRNs), and is dependent on MEC-4, a DEG/ENaC channel. We show that hemichannels containing the innexin protein UNC-7 are also essential for gentle touch in the TRNs, as well as harsh touch in both the TRNs and the PVD nociceptors. UNC-7 and MEC-4 do not colocalize, suggesting that their roles in mechanosensory transduction are independent. Heterologous expression of unc-7 in touch-insensitive chemosensory neurons confers ectopic touch sensitivity, indicating a specific role for UNC-7 hemichannels in mechanosensation. The unc-7 touch defect can be rescued by the homologous mouse gene Panx1 gene, thus, innexin/pannexin proteins may play broadly conserved roles in neuronal mechanotransduction.

scholarly journals Biophysical Principles of Ion-Channel-Mediated Mechanosensory Transduction

Cell Reports ◽  
2019 ◽  
Vol 29 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Charles D. Cox ◽  
Navid Bavi ◽  
Boris Martinac
Keyword(s):  
Ion Channel ◽  
Mechanosensory Transduction

Genetic approaches to mechanosensory transduction

1995 ◽  
Vol 5 (4) ◽  
pp. 443-448 ◽  
Author(s):  
Maurice Kernan ◽  
Charles Zuker
Keyword(s):  
Mechanosensory Transduction

scholarly journals Purinergic Mechanosensory Transduction and Visceral Pain

2009 ◽  
Vol 5 ◽  
pp. 1744-8069-5-69 ◽  
Author(s):  
Geoffrey Burnstock
Keyword(s):  
Visceral Pain ◽  
Mechanosensory Transduction

scholarly journals Distinct roles for innexin gap junctions and hemichannels in mechanosensation

2019 ◽  
Author(s):  
Denise S. Walker ◽  
William R. Schafer
Keyword(s):  
Blood Pressure ◽  
Pain Perception ◽  
Direct Role ◽  
Mechanosensory Transduction ◽  
Wide Range ◽  
Touch Receptor Neurons ◽  
Touch Sensitivity ◽  
Range Of Functions ◽  
Receptor Neurons ◽  
And Control

AbstractMechanosensation is central to a wide range of functions, including tactile and pain perception, hearing, proprioception, and control of blood pressure, but identifying the molecules underlying mechanotransduction has proved challenging. In Caenorhabditis elegans, the avoidance response to gentle body touch is mediated by 6 touch receptor neurons (TRNs), and is dependent on MEC-4, a DEG/ENaC channel. We show that hemichannels containing the innexin protein UNC-7 are also essential for gentle touch in the TRNs, as well as harsh touch in both the TRNs and the PVD nociceptors. UNC-7 and MEC-4 do not colocalize, suggesting that their roles in mechanosensory transduction are independent. Heterologous expression of unc-7 in touch-insensitive chemosensory neurons confers ectopic touch sensitivity, indicating a direct role for UNC-7 hemichannels in mechanosensation. The unc-7 touch defect can be rescued by the homologous mouse gene Panx1 gene, thus, innexin/pannexin proteins may play broadly conserved roles in neuronal mechanotransduction.

scholarly journals The Ca2+-activated cation channel TRPM4 is a positive regulator of pressure overload-induced cardiac hypertrophy

2020 ◽  
Author(s):  
Yang Guo ◽  
Ze-Yan Yu ◽  
Jianxin Wu ◽  
Hutao Gong ◽  
Scott Kesteven ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Transient Receptor Potential ◽  
Strong Predictor ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cation Channel ◽  
Systemic Hypertension ◽  
Mechanosensory Transduction ◽  
Trpm4 Channel

AbstractPathological left ventricular hypertrophy (LVH) is a consequence of pressure overload caused by systemic hypertension or aortic stenosis and is a strong predictor of cardiac failure and mortality. Understanding the molecular pathways in the development of pathological LVH may lead to more effective treatment. Here, we show that the transient receptor potential cation channel subfamily melastatin 4 (TRPM4) ion channel is an important contributor to the mechanosensory transduction of pressure overload that induces LVH. In mice with pressure overload induced by transverse aortic constriction (TAC) for two weeks, cardiomyocyte TRPM4 expression was reduced, as compared to control mice. Cardiomyocyte-specific TRPM4 inactivation reduced by ~50% the degree of TAC-induced LVH, as compared with wild type (WT). In WT mice, TAC activated the CaMKIIδ-HDAC4-MEF2A but not the calcineurin-NFAT-GATA4 pathway. In TRPM4 knock-out mice, activation of the CaMKIIδ-HDAC4-MEF2A pathway by TAC was significantly reduced. However, consistent with a reduction in the known inhibitory effect of CaMKIIδ on calcineurin activity, reduction in the CaMKIIδ-HDAC4-MEF2A pathway was associated with partial activation of the calcineurin-NFAT-GATA4 pathway. These findings indicate that the TRPM4 channel and its cognate signalling pathway are potential novel therapeutic targets for the prevention of pathological pressure overload-induced LVH.Significance statementPathological left ventricular hypertrophy (LVH) occurs in response to pressure overload and remains the single most important clinical predictor of cardiac mortality. Preventing pressure overload LVH is a major goal of therapeutic intervention. Current treatments aim to remove the stimulus for LVH by lowering elevated blood pressure or replacing a stenotic aortic valve. However, neither of these interventions completely reverses adverse cardiac remodelling. Although numerous molecular signalling steps in the induction of LVH have been identified, the initial step by which mechanical stretch associated with cardiac pressure overload is converted into a chemical signal that initiates hypertrophic signalling, remains unresolved. Here, we demonstrate that the TRPM4 channel is a component of the mechanosensory transduction pathway that ultimately leads to LVH.

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