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Selenoprotein T is required for pathogenic bacteria avoidance in Caenorhabditis elegans
Laura Romanelli-Cedrez1, Inés Carrera2, Lucía Otero2
1Worm Biology Laboratory, Institut Pasteur de Montevideo, Uruguay; Cátedra de Inmunología, Departamento de Biociencias, Facultad de Química, Universidad de la República, Montevideo, Uruguay.
Free Radical Biology & Medicine
|March 29, 2017
Summary
Selenoprotein T (SELENOT) in C. elegans, specifically SELT-1.1, acts as a redox transducer essential for stress response and sensory behaviors like pathogen avoidance and nociception.
Area of Science:
- Biochemistry
- Molecular Biology
- Neuroscience
Background:
- Selenoprotein T (SELENOT) is an ER-associated redoxin with known roles in mammalian Ca2+ homeostasis, antioxidant defense, and neuroendocrine functions.
- The precise function of SELENOT in whole multicellular organisms remains incompletely understood.
- C. elegans possesses two SELENOT orthologs, SELT-1.1 and SELT-1.2, which have evolved distinct redox motifs and localization patterns.
Purpose of the Study:
- To investigate the function of SELENOT orthologs (SELT-1.1 and SELT-1.2) in the model organism C. elegans throughout its life cycle.
- To understand the evolutionary events shaping SELENOT proteins in nematodes.
- To determine the role of SELT-1.1 and SELT-1.2 in stress response, sensory perception, and overall organismal fitness.
Main Methods:
- Comparative analysis of SELENOT orthologs in C. elegans, focusing on sequence evolution (Sec→Cys replacement, gene duplication).
- Subcellular localization studies (ER, cytoplasm) and cell-type specific expression analysis (nervous system, AWB neurons).
- Phenotypic analysis of single and double mutants (selt-1.1, selt-1.2) under normal conditions, oxidative stress (rotenone), and in response to specific stimuli (bacterial pathogens, 2-nonanone).
Main Results:
- Evolutionary analysis revealed Sec→Cys replacement and gene duplication as key events in nematode SELENOT evolution.
- SELT-1.1 localizes to the ER and is broadly expressed, while SELT-1.2 is restricted to AWB neuron cytoplasm.
- selt-1.1 mutants exhibit compromised resistance to rotenone-induced oxidative stress and impaired avoidance behaviors towards bacterial pathogens and 2-nonanone.
Conclusions:
- SELT-1.1 functions as a redox transducer crucial for nociception and organismal fitness in C. elegans.
- SELT-1.2's specific role remains to be fully elucidated, but its localization suggests neuronal functions.
- C. elegans provides a valuable model for studying SELENOT-dependent processes, particularly in the context of stress and sensory biology.
