Dr. Lakshya Bajaj
Associate Professor

Contact Info
- University of Puerto Rico
Medical Sciences Campus
P.O. Box 365067
San Juan, PR 00936-5067 - 787-758-2525 Ext. 1300 (office)/1365 (lab)
Education
- B.D.S. (Dental Medicine) Maharishi Dayanand University, Haryana, India
- M.S. (Human Genetics), Tulane University, New Orleans, LA
- Ph.D. (Human and Molecular Genetics), Baylor College of Medicine, Houston, TX
- Postdoctoral Fellowship (Genetics), Harvard Medical School, Boston, MA
RESEARCH AREAS
- Ribo-Proteostasis in Neurodegenerative Diseases
- Biomolecular Condensates in Neurodegenerative Diseases
- Neuronal Mosaicism
- 3D-Organoids for Neurodegenerative Diseases Modelling
RESEARCH INTEREST
Our lab is dedicated to exploring the molecular mechanisms behind neurodegenerative diseases, with a central focus on ribo-proteostasis—the intricate balance between RNA metabolism and protein homeostasis. We investigate how disruptions in RNA metabolism, protein trafficking, and cellular quality control lead to the formation of membrane-less biomolecular condensates, such as stress granules. Of particular interest is understanding how these dynamic, liquid-like stress granules transition into solid, toxic aggregates in diseases like ALS and Alzheimer’s.
Building on this foundation, our lab employs cutting-edge techniques, including 3D organoids for modeling various neurodegenerative diseases and high-throughput techniques such as proteomics, RNA sequencing, single-cell spatial mapping, and RNA structural probing (DMS/SHAPE) to dissect complex gene regulatory cellular mechanisms to uncover the broader implications of these processes in human health. Our lab thus strives to understand the fundamental biology of RNA metabolism and protein homeostasis, while also addressing how dysregulations in these processes can lead to disease pathogenesis thus offering potential biomarkers and therapeutic targets for intervention.
Lab Website– www.bajaj-lab.com
PUBLICATIONS
- Calpain activity is negatively regulated by a KCTD7-Cullin-3 complex via non-degradative ubiquitinationJaiprakash Sharma, Shalaka Mulherkar, Uan-I Chen, Yan Xiong, Lakshya Bajaj, Byoung-Kyu Cho, Young Ah Goo, Hon-Chiu Eastwood Leung, Kimberley F. Tolias and Marco SardielloCell Discovery. 2023 Mar 24;9(1):32.doi: 10.1038/s41421-023-00533-3.
- ZSP-1 is a Z granule surface protein required for Z granule fluidity and germline immortality in Caenorhabditis elegans.Wan G, Bajaj L, Fields B, Dodson AE, Pagano D, Fei Y, Kennedy S.EMBO J. 2021 Feb 1;40(3):e105612. doi: 10.15252/embj.2020105612.
- A CLN6-CLN8 complex recruits lysosomal enzymes at the ER for Golgi transfer.Bajaj L, Sharma J, di Ronza A, Zhang P, Eblimit A, Pal R, Roman D, Collette JR, Booth C, Chang KT, Sifers RN, Jung SY, Weimer JM, Chen R, Schekman RW, Sardiello M.J Clin Invest. 2020 Aug 3;130(8):4118-4132. doi: 10.1172/JCI130955.
- Lysosome biogenesis in health and disease.Bajaj L, Lotfi P, Pal R, Ronza AD, Sharma J, Sardiello M.J Neurochem. 2019 Mar;148(5):573-589. doi: 10.1111/jnc.14564. Epub 2018 Oct 18.
- CLN8 is an endoplasmic reticulum cargo receptor that regulates lysosome biogenesis.di Ronza A, Bajaj L, Sharma J, Sanagasetti D, Lotfi P, Adamski CJ, Collette J, Palmieri M, Amawi A, Popp L, Chang KT, Meschini MC, Leung HE, Segatori L, Simonati A, Sifers RN, Santorelli FM, Sardiello M.Nat Cell Biol. 2018 Dec;20(12):1370-1377. doi: 10.1038/s41556-018-0228-7.
- TFEB enhances astroglial uptake of extracellular tau species and reduces tau spreading.Martini-Stoica H, Cole AL, Swartzlander DB, Chen F, Wan YW, Bajaj L, Bader DA, Lee VMY, Trojanowski JQ, Liu Z, Sardiello M, Zheng H.J Exp Med. 2018 Sep 3;215(9):2355-2377. doi: 10.1084/jem.20172158.
- mTORC1-independent TFEB activation via Akt inhibition promotes cellular clearance in neurodegenerative storage diseases.Palmieri M, Pal R, Nelvagal HR, Lotfi P, Stinnett GR, Seymour ML, Chaudhury A, Bajaj L, Bondar VV, Bremner L, Saleem U, Tse DY, Sanagasetti D, Wu SM, Neilson JR, Pereira FA, Pautler RG, Rodney GG, Cooper JD, Sardiello M.Nat Commun. 2017 Feb 6;8:14338. doi: 10.1038/ncomms14338.
- NADPH oxidase promotes Parkinsonian phenotypes by impairing autophagic flux in anmTORC1-independent fashion in a cellular model of Parkinson’s disease.Pal R, Bajaj L, Sharma J, Palmieri M, Di Ronza A, Lotfi P, Chaudhury A, Neilson J, Sardiello M, Rodney GG.Sci Rep. 2016 Mar 10;6:22866. doi: 10.1038/srep22866.