Pant A et al. (2016) Exp Gerontol "Corrigendum to "Beta-caryophyllene modulates expression of stress response genes and mediates longevity in Caenorhabditis elegans" [Exp. Gerontol. 57 (2014) 81-95]."

Saikia SK, Pant A, Shukla V, Asthana J, Pandey R, Akhoon BA

[Exp Gerontol, 2016]

The authors would like to acknowledge the contribution of Vikas Mishra for this article.Therefore the correct authorship of this paper at the time should have read as follows:Aakanksha Pant*, Vikas Mishra*, Shilpi K. Saikia, Virendra Shukla, Jyotsna Asthana, Bashir A. Akhoon, Rakesh Pandey.(* authors with equal contribution).The authors would like to apologize for any inconvenience caused.

Brar, Harjot Kaur et al. (2021) International Worm Meeting "Dendrite regeneration in PVD neuron is controlled by the RAC GTPase CED-10 and the RhoGEF TIAM-1"

Ghosh-Roy, Anindya, Dey, Swagata, Brar, Harjot Kaur, Pandey, Devashish, Bhardwaj, Smriti, Dey, Shirshendu

[International Worm Meeting, 2021]

Neurons are vulnerable to physical insults which compromise the integrity of both dendrites and axons. Unlike well characterized axon regeneration, our knowledge in dendrite regeneration is limited. To understand the mechanisms of dendrite regeneration, we used PVD neurons with stereotyped branched dendrites. Using femtosecond laser, we severed the primary dendrites and axon of this neuron. After the primary dendrite was severed near the cell body, we observed a sprouting of new branches from the cut site within 3 hours. By 24 hours, the primary dendrite regrew to cover the original territory in complex pattern unlike the uninjured dendrites. We quantified the regeneration in broadly two aspects- the territory covered and fusion phenomena (Oren-Suissa et al.,2017, Kravtsov et al.,2017). Axon injury causes a retraction of the severed end followed by a Dual leucine zipper kinase-1(DLK-1) dependent regrowth from the severed end or conversion of neighboring dendrite to axon. However, Dendrite regeneration was independent of DLK-1 and other conventional axon regeneration pathways including cAMP elevation, let-7 miRNA, Akt-1 and Phosphatidyl serine exposure/PS. Among various candidates tested, ced-10 mutants showed a defect in dendrite regeneration. It is a RAC GTPase involved in regulation of neuronal cytoskeleton and cell engulfment. Cell-specific rescue experiments suggest that cell-autonomous and epidermal expression of CED-10 is required for dendrite regrowth and fusion, respectively. Moreover, the PVD-specific expression of an activated version of CED-10 led to both increased branching and fusion. We ventured further to find the upstream players which can control the function of RAC GTPase in dendrite regeneration. We found out that the TIAM-1 RhoGEF is required for dendrite regeneration and the activated CED-10 can bypass the requirement of TIAM-1 in dendrite regrowth. Our work provides a framework for understanding the cellular mechanism of dendrite regeneration using PVD model. Reference: Oren-Suissa, M., T. Gattegno, V. Kravtsov and B. Podbilewicz, 2017 Extrinsic Repair of Injured Dendrites as a Paradigm for Regeneration by Fusion in Caenorhabditis elegans. Genetics 206: 215-230. Kravtsov, V., M. Oren-Suissa and B. Podbilewicz, 2017 The fusogen AFF-1 can rejuvenate the regenerative potential of adult dendritic trees by self-fusion. Development 144: 2364-2374.

Singh, Jatinder et al. (2013) International Worm Meeting "Understanding the auto-receptor component of the DOP-2 signal transduction pathway in modulating dopamine release."

Clark, Crystal, Han, Ping, Harbinder, Singh, King, Roderick, Singh, Jatinder

[International Worm Meeting, 2013]

Modulating the levels of dopamine is important in a wide range of physiological and neural functions We are interested in understanding the auto-receptor functional component of the DOP-2 receptor in modulating dopamine release. Our results indicate that mutants in the dop-2 pathway habituate faster and display deficits in associative learning. In order to dissect function(s) of individual splice variants we also present preliminary results on the differential levels of alternatively spliced forms of the dop-2 transcript. Binding of dopamine to its G-protein coupled seven-transmembrane D1-like or D2-like dopamine receptors can trigger antagonistic signal transduction cascades. Four dopamine receptors have been identified in the C. elegans genome: DOP-1 is a D1-like receptor, DOP-2 and DOP-3 are D2-like receptors, and DOP-4 is an invertebrate specific receptor. DOP-2 is expressed in the 8 dopaminergic neurons in the hermaphrodite (plus additional neurons mainly in the male tail). The dop-2 transcript is spliced into 4 alternate forms and its protein product may play a role in modulating levels of dopamine released by acting as an auto-receptor. Recent work in our lab has shown that DOP-2 physically interacts with GPA-14, an inhibitory G-alpha subuniti, and that both dop-2 and gpa-14 deletion mutant habituate at a significantly faster rate as compared to wild-type. Furthermore, gpa-14 deletion mutants also show associative learning deficits similar to those previously reported for dop-2 deletion. In order to characterize the downstream molecular components of the DOP-2 auto-receptor function we are characterizing trp-4 loss-of-function mutants. Key references: Suo et al. (2003) J Neurochem. 86: 869-878; Kindt et al. (2007) Neuron. 55(4):662-676; Voglis and Tavernarakis (2008). EMBO J. 27: 3288-3299; Pandey and Harbinder (2012) J. Molecular Signaling. 7: 1-10.