Vandita Gorla

University of Southern California

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Tripti Nair

National Institute of Immunology

Sean P. Curran

University of Southern California

Chris Turner

University of Southern California

Marisa Gaglio

University of Southern California

Brandy Weathers

University of Southern California

James D. Nhan

University of Southern California

Carmen M. Ramos

University of Southern California

Nicole L. Stuhr

University of Southern California

Carmen Ramos

University of Southern California

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University of Southern California

Massachusetts General Hospital

Southern California University for Professional Studies

University Hospitals Coventry and Warwickshire NHS Trust

University College London Hospitals NHS Foundation Trust

National Hospital for Neurology and Neurosurgery

University College London

South Texas Blood and Tissue Center

University of Surrey

University Hospital Coventry

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SKN-1 isoform-c is essential for

PubMed (2024)

Tripti Nair Carmen M. Ramos Chris Turner Vandita Gorla Marisa Gaglio

The transcription factor SKN-1 in

10.17912/micropub.biology.001205

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PATHOGEN APATHY RESULTING FROM SKN-1 ACTIVATION: A MARK OF RESILIENCE OR A RATTLED GUT FEELING?

Innovation in Aging (2023)

Tripti Nair Brandy Weathers Nicole L. Stuhr James D. Nhan Vandita Gorla

Abstract Innate immunity is a key driver in promoting survival against xenobiotic stressors and hostile environments and an appropriate immune response is essential to organismal health across lifespan. Caenorhabditis elegans encounter pathogens in their natural environment and initiate cytoprotective and immune responses that can have long-lasting effects on health, even after the pathogen has been neutralized. Pseudomonas aeruginosa (PA14) is an opportunistic pathogen that is lethal to C. elegans with prolonged exposure. C. elegans employ multiple defense mechanisms to ensure survival upon exposure to pathogens to defend against the current infection and to avoid continued exposure, including activation of the key cytoprotective transcription factor SKN-1 (mammalian homologue Nrf2). Although wild type C. elegans quickly learn to avoid pathogens, our current work documents a peculiar apathy to pathogen in animals with constitutive activation of SKN-1. The outcome is surprising as the role of SKN-1 is to protect an animal from intracellular and environmental insults. This behavior is mediated by tissue specific actions of SKN-1 that initiate cell non-autonomous responses for pathogen avoidance, survival, and metabolic adaptation. Based on transcriptional signature of animals with SKN-1 activation upon exposure to PA14 we observed that the apathy behavior is independent of somatic lipid depletion, thus uncoupling these two exceptional physiological responses. Further, we define the role of neurosignalling molecules in the gut-brain axis that drive the apathy response to pathogens. Our work reveals new insights into how animals perceive pathogens in the environment and subsequently alter behavior and cellular programs to promote survival.

Apathy

WRKY protein domain

10.1093/geroni/igad104.3514

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SKN-1 ISOFORM-C IS ESSENTIAL FOR C. ELEGANS DEVELOPMENT

Innovation in Aging (2024)

Marisa Gaglio Vandita Gorla Tripti Nair Carmen Ramos Chris Turner

Abstract The transcription factor SKN-1 in Caenorhabditis elegans is a critical regulator of various biological processes, impacting development, diet and immune responses, cellular detoxification, and lipid metabolism; thereby playing a pivotal role in regulating the health and lifespan of the organism. The primary isoforms of SKN-1 (SKN-1a, SKN-1b, and SKN-1c) exhibit distinct functions resembling mammalian Nrf transcription factors. This study investigates the specific role of the SKN-1c isoform in development by generating mutants with targeted missense mutations in the skn-1c and skn-1a isoforms. The skn-1c Met1Ala mutants, which replaces a start methionine with alanine, renders SKN-1c non-functional while preserving other isoforms, produced inviable embryos, requiring a balancer chromosome for proper embryonic development. In contrast, skn-1a Met1Ala mutants, which replaces the start methionine with alanine for this isoform, displayed normal embryonic development and hatching. Moreover, the data suggest that SKN-1c plays a crucial role in embryonic development, as strains without maternally deposited SKN-1c lead to embryos that are developmentally arrested. Together, these findings contribute to our understanding of SKN-1c’s specific role in influencing embryogenesis and development in C. elegans.

10.1093/geroni/igae098.3718

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