Page Not Found
Page not found. Your pixels are in another canvas.
Sitemap
A list of all the posts and pages found on the site. For you robots out there is an XML version available for digesting as well.
Pages
About
About
Page not in menu
This is a page not in th emain menu
Posts
portfolio
Portfolio item number 1
Short description of portfolio item number 1
Portfolio item number 2
Short description of portfolio item number 2
publications
Oscillating PDF in termini of circadian pacemaker neurons and synchronous molecular clocks in downstream neurons are not sufficient for sustenance of activity rhythms in constant darkness
Published in PLoS ONE, 2017
In Drosophila, neuropeptide Pigment Dispersing Factor (PDF) is expressed in small and large ventral Lateral Neurons (sLNv and lLNv), among which sLNv are critical for activity rhythms in constant darkness. Studies show that this is mediated by rhythmic accumulation and likely secretion of PDF from sLNv dorsal projections, which in turn synchronises molecular oscillations in downstream circadian neurons. Using targeted expression of a neurodegenerative protein Huntingtin in LNv, we evoke a selective loss of neuropeptide PDF and clock protein PERIOD from sLNv soma. However, PDF is not lost from sLNv dorsal projections and lLNv. These flies are behaviourally arrhythmic in constant darkness despite persistence of PDF oscillations in sLNv dorsal projections and synchronous PERIOD oscillations in downstream circadian neurons. We find that PDF oscillations in sLNv dorsal projections are not sufficient for sustenance of activity rhythms in constant darkness and this is suggestive of an additional component that is possibly dependent on sLNv molecular clock and PDF in sLNv soma. Additionally, despite loss of PERIOD in sLNv, their activity rhythms entrain to light/dark cycles indicating that sLNv molecular clocks are not necessary for entrainment. Under constant light, these flies lack PDF from both soma and dorsal projections of sLNv, and when subjected to light/dark cycles, show morning and evening anticipation and accurately phased morning and evening peaks. Thus, under light/dark cycles, PDF in sLNv is not necessary for morning anticipation.
Recommended citation: Pavitra Prakash, Aishwarya Nambiar, and Sheeba Vasu. "Oscillating PDF in termini of circadian pacemaker neurons and synchronous molecular clocks in downstream neurons are not sufficient for sustenance of activity rhythms in constant darkness." PLoS One 12.5 (2017): e0175073. https://doi.org/10.1371/journal.pone.0175073 https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0175073
Hsp40 overexpression in pacemaker neurons delays circadian dysfunction in a Drosophila model of Huntington’s disease
Published in Disease Models & Mechanisms (DMM), 2022
Circadian disturbances are early features of neurodegenerative diseases, including Huntington’s disease (HD). Emerging evidence suggests that circadian decline feeds into neurodegenerative symptoms, exacerbating them. Therefore, we asked whether known neurotoxic modifiers can suppress circadian dysfunction. We performed a screen of neurotoxicity-modifier genes to suppress circadian behavioural arrhythmicity in a Drosophila circadian HD model. The molecular chaperones Hsp40 and HSP70 emerged as significant suppressors in the circadian context, with Hsp40 being the more potent mitigator. Upon Hsp40 overexpression in the Drosophila circadian ventrolateral neurons (LNv), the behavioural rescue was associated with neuronal rescue of loss of circadian proteins from small LNv soma. Specifically, there was a restoration of the molecular clock protein Period and its oscillations in young flies and a long-lasting rescue of the output neuropeptide Pigment dispersing factor. Significantly, there was a reduction in the expanded Huntingtin inclusion load, concomitant with the appearance of a spot-like Huntingtin form. Thus, we provide evidence implicating the neuroprotective chaperone Hsp40 in circadian rehabilitation. The involvement of molecular chaperones in circadian maintenance has broader therapeutic implications for neurodegenerative diseases.
Recommended citation: Pavitra Prakash, Arpit Kumar Pradhan, Vasu Sheeba; Hsp40 overexpression in pacemaker neurons delays circadian dysfunction in a Drosophila model of Huntington's disease. Dis Model Mech 1 June 2022; 15 (6): dmm049447. doi: https://doi.org/10.1242/dmm.049447 https://journals.biologists.com/dmm/article/15/6/dmm049447/275822/Hsp40-overexpression-in-pacemaker-neurons-delays
First person – Pavitra Prakash
Published in Disease Models & Mechanisms (DMM), 2022
First Person is a series of interviews with the first authors of a selection of papers published in Disease Models & Mechanisms, helping early-career researchers promote themselves alongside their papers. Pavitra Prakash is first author on ‘Hsp40 overexpression in pacemaker neurons delays circadian dysfunction in a Drosophila model of Huntington’s disease’, published in DMM. Pavitra is a PhD student in the lab of Dr Sheeba Vasu at Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, India, investigating the bi-directional relationship between circadian health and neurodegenerative diseases.
Recommended citation: First person – Pavitra Prakash. Dis Model Mech 1 June 2022; 15 (6): dmm049678. doi: https://doi.org/10.1242/dmm.049678 https://journals.biologists.com/dmm/article/15/6/dmm049678/275826/First-person-Pavitra-Prakash
talks
teaching
Teaching experience 1
Undergraduate course, University 1, Department, 2014
This is a description of a teaching experience. You can use markdown like any other post.