Biraj Mahato

University of Southern California

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Samit Adhya

Indian Institute of Chemical Biology

Subrata Batabyal

Scope Group (United States)

Samarendra Mohanty

Scope Group (United States)

Sai H. Chavala

University of North Texas

Aiguo Ni

University of North Texas

Yan Fan

University of North Texas Health Science Center

Soumen Paul

University of Kansas Medical Center

Rafal Farjo

Eye Center

Houssam Al-Saad

Scope Group (United States)

Sukanta Jash

Women & Infants Hospital of Rhode Island

Cooperative Institutions

University of North Texas

University of North Texas Health Science Center

University of Kansas Medical Center

University of Kansas

Indian Institute of Chemical Biology

Institute for Reproductive Health

Scope Group (United States)

Smith-Kettlewell Eye Research Institute

National Institutes of Health

University of Michigan–Ann Arbor

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Pharmacologic fibroblast reprogramming into photoreceptors restores vision

Nature (2020)

Biraj Mahato Koray Dogan Kaya Yan Fan Nathalie Sumien Ritu A. Shetty

Reprogramming

10.1038/s41586-020-2201-4

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Citations (89)

MDM2 inhibition suppresses NF-κB-mediated inflammation in retinal pigment epithelium cells

Investigative Ophthalmology & Visual Science (2016)

Biraj Mahato

Source

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Regulation of Mitochondrial Function and Cellular Energy Metabolism by Protein Kinase C-λ/ι: A Novel Mode of Balancing Pluripotency

Stem Cells (2014)

Biraj Mahato Pratik Home Ganeshkumar Rajendran Arindam Paul Biswarup Saha

Pluripotent stem cells (PSCs) contain functionally immature mitochondria and rely upon high rates of glycolysis for their energy requirements. Thus, altered mitochondrial function and promotion of aerobic glycolysis are key to maintain and induce pluripotency. However, signaling mechanisms that regulate mitochondrial function and reprogram metabolic preferences in self-renewing versus differentiated PSC populations are poorly understood. Here, using murine embryonic stem cells (ESCs) as a model system, we demonstrate that atypical protein kinase C isoform, PKC lambda/iota (PKCλ/ι), is a key regulator of mitochondrial function in ESCs. Depletion of PKCλ/ι in ESCs maintains their pluripotent state as evident from germline offsprings. Interestingly, loss of PKCλ/ι in ESCs leads to impairment in mitochondrial maturation, organization, and a metabolic shift toward glycolysis under differentiating condition. Our mechanistic analyses indicate that a PKCλ/ι-hypoxia-inducible factor 1α-PGC1α axis regulates mitochondrial respiration and balances pluripotency in ESCs. We propose that PKCλ/ι could be a crucial regulator of mitochondrial function and energy metabolism in stem cells and other cellular contexts.

Anaerobic glycolysis

10.1002/stem.1817

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Citations (30)

Inhibition of Noncanonical Murine Double Minute 2 Homolog Abrogates Ocular Inflammation through NF-κB Suppression

American Journal Of Pathology (2018)

Yan Fan Wei Zhang Aiguo Ni Biraj Mahato Sai H. Chavala

10.1016/j.ajpath.2018.05.017

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Vision rescue via chemically engineered endogenous retinal ganglion cells

bioRxiv (Cold Spring Harbor Laboratory) (2023)

Rana Muhammad Shoaib Aregnazan Sandrosyan Biraj Mahato

Abstract Loss of retinal ganglion cells (RGCs) is the final common end point for many optic neuropathies, ultimately leading to irreversible vision loss. Endogenous RGC regeneration from Müller cells presents a promising approach to treat these diseases, but mammalian retinas lack regenerative capacity. Here, we report a small molecule cocktail that causes endogenous Müller cell proliferation, migration, and specification to newly generated chemically induced RGCs (CiRGCs) in NMDA injured mice retina. Notably, regenerated CiRGCs extend axons towards optic nerve, and rescue vision post-NMDA treatment. Moreover, we successfully reprogrammed human primary Müller glia and fibroblasts into CiRGCs using this chemical-only approach, as evidenced by RGC-specific gene expression and chromatin signature. Additionally, we show that interaction between SOX4 and NF-kB determine CiRGC fate from Müller cells. We anticipate endogenous CiRGCs would have therapeutic potential in rescuing vision for optic nerve diseases.

10.1101/2023.12.27.572921

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Endosome Independent ‐ Vesicular Transport and Targeting of the Leishmania RNA Import Complex to Mammalian Mitochondria in Vivo and in Vitro

The FASEB Journal (2015)

Joyita Mukherjee Biraj Mahato Sandip Koley Samit Adhya

The multi subunit RNA Import Complex (RIC) from the protozoal parasite Leishmania tropica is taken up by mammalian cells and trafficked to mitochondria, with functional RNA delivered to the matrix by an unknown mechanism. By live cell imaging of siRNA mediated knockdown cells we showed that intracellular vesicular transport of the ribonuclear protein complex is dependent on caveolin1, dynamin2 and filaminA but independent of components of the endosomal pathway such as EEA1, Rab5 or Rab7. Moreover, mitochondrial targeting was dependent on TOM20 and TOM22, two components of the outer membrane machinery. By immuno‐selection we could distinguish two types of RNA loaded cytoplasmic vesicles, one containing caveolar components and the other lacking them. In vitro, transfer of RNP from the caveolin negative transport vesicles to mitochondria was dependent on ATP and on TOM22. RIC was transferred to TOM20 deficient mitochondrial membrane but the RNA was not imported into the matrix. These results imply that (1) endosomes are not involved in RIC trafficking and novel interactions between vesicle associated RIC and (2) TOM20 and TOM22 are required for transfer and positioning of RIC on the mitochondrial surface. Supported By: Project Bend of the Council of Scientific and Industrial Research. Ref: Mukherjee, J. (2014). Vesicular transport of a ribonucleoprotein to mitochondria. Biology Open, doi: 10.1242/bio.20149076.

Vesicular Transport Proteins

Transport protein

10.1096/fasebj.29.1_supplement.574.4

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RNA-mediated restoration of mitochondrial function in cells harboring a Kearns Sayre Syndrome mutation

Mitochondrion (2011)

Biraj Mahato Sukanta Jash Samit Adhya

MT-RNR1

10.1016/j.mito.2011.03.006

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Citations (21)