# Calcineurin A/TAX-6 signaling inhibits noxious heat-evoked nuclear accumulation of CMK-1 in the FLP thermo-nociceptive neurons of Caenorhabditis elegans

## TL;DR

This study explores how a signaling pathway in C. elegans affects the movement of a protein into the nucleus of heat-sensing neurons when exposed to high temperatures.

## Contribution

The paper identifies a new regulatory mechanism involving Calcineurin A/TAX-6 in modulating thermo-nociceptive plasticity in C. elegans.

## Key findings

- Calcineurin A/TAX-6 activation blocks CMK-1 nuclear translocation in FLP neurons at 28°C.
- Loss of Calcineurin A/TAX-6 slightly enhances CMK-1 nuclear accumulation.
- The signaling pathway negatively regulates CMK-1 nuclear accumulation.

## Abstract

Calcium signaling is central to neural plasticity. In

C. elegans

, the CaM kinase I/
CMK-1
and the phosphatase Calcineurin A/
TAX-6
antagonistically regulate thermo-nociceptive behavior via partially overlapping neuronal circuits. Following prolonged exposure to noxious temperature (90 min, 28°C)
CMK-1
localization shifts from cytoplasmic to nuclear in FLP neurons, which reduces behavioral responsiveness. We examined whether Calcineurin A/
TAX-6
influences this process. Using
CMK-1
::mNeonGreen, we found that Calcineurin A/
TAX-6
activation blocks, while its loss slightly enhances,
CMK-1
nuclear translocation at 28°C. These results reveal that Calcineurin A/
TAX-6
signaling negatively regulates
CMK-1
nuclear accumulation, providing a potential mechanism for opposing modulation of thermo-nociceptive plasticity.