Leucine Regulates Neuronal Health During Nutrient Deprivation in Caenorhabditis elegans
- 1National Centre for Biological Sciences - TIFR
Abstract
Alterations in nutrient availability induce changes in neuronal structure and connectivity across species, ultimately leading to nervous system plasticity and behavioural changes. However, it remains unclear how prolonged acute nutrient deprivation affects the integrity and function of the nervous system. Using the nematode Caenorhabditis elegans, we uncovered that prolonged macronutrient deprivation profoundly impacts neuronal health. Across developmental stages, multiple sensory neuron classes in the C. elegans nervous system, including polymodal IL2, volatile odor-sensing AWB and AWC, and CO2-sensing BAG neurons, display extensive dendritic and axonal blebbing, severely disorganized dendritic, axonal, and cell body morphologies, and severely disrupted chemical and electrical synaptic organization during prolonged nutrient deprivation. The severity of these defects increases progressively with the duration of nutrient deprivation, ultimately affecting animal behaviours. Our results show that the availability of a particular macronutrient, specifically the branched-chain amino acid leucine alone, in the absence of any other macronutrients, although insufficient to support animal growth, is sufficient to completely prevent nutrient-deprivation-mediated neuronal damage and the decline in animal behavioural responses. Moreover, leucine supplementation alone is sufficient to reverse nutrient-deprivation-mediated neuronal abnormalities. These findings suggest that the availability of leucine, rather than absolute caloric intake, is crucial for maintaining neuronal health and function under adverse conditions.
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BibTeX
@misc{sudhanand2026leucine,
title = {{Leucine Regulates Neuronal Health During Nutrient Deprivation in Caenorhabditis elegans}},
author = {M. Sudhanand and A. Sahu and J. Desai and U. Bandyopadhyay and A. Bhattacharya},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.04.748567},
url = {https://www.biorxiv.org/content/10.64898/2026.09.04.748567v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Leucine Regulates Neuronal Health During Nutrient Deprivation in Caenorhabditis elegans
AU - M. Sudhanand
AU - A. Sahu
AU - J. Desai
AU - U. Bandyopadhyay
AU - A. Bhattacharya
PY - 2026
DA - 2026/09/04
PB - bioRxiv
DO - 10.64898/2026.09.04.748567
UR - https://www.biorxiv.org/content/10.64898/2026.09.04.748567v1
AB - Alterations in nutrient availability induce changes in neuronal structure and connectivity across species, ultimately leading to nervous system plasticity and behavioural changes. However, it remains unclear how prolonged acute nutrient deprivation affects the integrity and function of the nervous system. Using the nematode Caenorhabditis elegans, we uncovered that prolonged macronutrient deprivation profoundly impacts neuronal health. Across developmental stages, multiple sensory neuron classes in the C. elegans nervous system, including polymodal IL2, volatile odor-sensing AWB and AWC, and CO2-sensing BAG neurons, display extensive dendritic and axonal blebbing, severely disorganized dendritic, axonal, and cell body morphologies, and severely disrupted chemical and electrical synaptic organization during prolonged nutrient deprivation. The severity of these defects increases progressively with the duration of nutrient deprivation, ultimately affecting animal behaviours. Our results show that the availability of a particular macronutrient, specifically the branched-chain amino acid leucine alone, in the absence of any other macronutrients, although insufficient to support animal growth, is sufficient to completely prevent nutrient-deprivation-mediated neuronal damage and the decline in animal behavioural responses. Moreover, leucine supplementation alone is sufficient to reverse nutrient-deprivation-mediated neuronal abnormalities. These findings suggest that the availability of leucine, rather than absolute caloric intake, is crucial for maintaining neuronal health and function under adverse conditions.
ER -