1. Mechanistic role of extracellular ATP on activation of P2X2 receptor ion channels in the hearing organ.
2. Physiological relevance of stria vascularis Calcium transporters and ion channels contributing to the development of hearing loss (age-related and permanent noise-induced).
3. Signalling mechanism of cyclic molecules in sensory hair cells underlying low-frequency hearing.
How radixin modulates outer hair cell stereocilia function and is a part of the amplification in the hearing organ?
In this project as a postdoc I investigated ‘the role of radixin protein in the potential modulation of outer hair cell stereocilia function.’
Significance: A new mechanistic role of radixin protein contributing to the control of hearing sensitivity is described here. We show that hearing loss in people with radixin gene mutations is caused by alterations in the sensory hair cell mechanics. Radixin blockade increases sound-evoked stereocilia and electrically evoked hair cell motion which is consistent with the reduced stiffness of stereocilia. It severely affects the electrical responses and hearing sensitivity in vivo suggesting radixin is important for regulating mechanically sensitive channels function and is a part of the cochlear amplification. These physiological responses strongly contribute in the maintenance of hearing sensitivity explaining the hearing loss that develops in the early postnatal period in RDX mutations patient.
1. Investigating the Role of Radixin in Modulation of Stereocilia Length and Stiffness., AIP Conference Proceedings, 2018.
2. Radixin modulates the function of outer hair cell stereocilia., Nature Communications Biology, 2020. (Under revision)
In addition to my postdoc project I worked in parallel for five months on another collaborative project titled ‘Control of hearing sensitivity by tectorial membrane Calcium’.
Significance: A new mechanism that contributes to control of hearing sensitivity is described here. We show that an accessory structure in the hearing organ, the tectorial membrane, strongly affects the function of inner ear sensory cells by storing calcium ions. When the calcium store is depleted, by brief exposure to rock-concert-level sounds or by the introduction of calcium chelators, the sound-evoked responses of the sensory cells decrease. Upon restoration of calcium storage, sensory cell function returns. This previously unknown mechanism contributes to explaining the temporary numbness in the ear that follows from listening to sounds that are too loud – a phenomenon that most people experience at some point in their lives.
Paper: Control of hearing sensitivity by tectorial membrane calcium., PNAS, 2019.
I obtained my Doctoral degree (July 2014) in the major subject area of Cellular Neurophysiology in July 2014 at Medizinische Hochschule Hannover (MHH) and Master’s degree in Molecular Biophysics in August 2010 at Jacobs University Bremen (JUB) in Germany.
The title of my doctoral thesis project was ‘5-HT7 and 5-HT1A receptor oligomerization regulates cAMP-based signaling’.
1. Serotonin receptor oligomerization regulates cAMP-based signaling., Journal of Cell Science, 2019.
2. Biophysical application of quantitative spectral-based linear unmixing and ratiometric FRET., Journal of Microscopy, 2020.
3. Analysis of receptor-receptor interaction by combined application of FRET and microscopy., Methods in Cell Biology, 2013.
In addition to my doctoral thesis project I worked in parallel for nine months on another collaborative project titled ‘Attenuated palmitoylation of serotonin receptor 5-HT1A in brain affects receptor functions and triggers depressive symptoms’.
Paper: Attenuated palmitoylation of serotonin receptor 5-HT1A affects receptor function and contributes to depression-like behaviors., Nature Communications, 2019.