Thermal Stress Disrupts Gut Microbiota, Induces Oxidative DNA Damage, and Modulates Immune and Stress-Related Gene Expression in the Red Sea Urchin ( Loxechinus albus ).

Abstract

The red sea urchin Loxechinus albus is a species of high commercial importance in Chilean aquaculture, whose performance is strongly influenced by environmental conditions such as temperature. The gut microbiota plays a central role in host physiology; however, its interaction with stress-induced molecular responses remains poorly understood. This study evaluated the effects of thermal stress on food consumption, gut microbial composition, oxidative status, and immune- and stress-related gene expressions in L. albus gut. Sea urchins were exposed to control (16 °C) and elevated temperature (22 °C) conditions for 7 and 14 days. Gut microbiota was characterized using 16S rRNA sequencing, while oxidative damage to DNA and proteins was quantified. Gene expression analyses targeted markers of apoptosis ( casp3 , casp10 , bak1 ), cellular growth ( mtor , raptor ), stress response ( hsp70 ), and immune regulation ( nfκb , foxo ). Thermal stress induced a marked reduction in microbial alpha diversity and promoted a shift toward opportunistic taxa. Heat-stressed individuals exhibited significantly increased oxidative DNA damage, whereas protein oxidation remained unchanged. Gene expression analyses revealed early upregulation of casp3 , casp10 , nfκb , foxo , and hsp70 , suggesting activation of apoptotic, immune, and stress-response pathways. In contrast, bak1 , mtor , and raptor showed limited or no significant modulation. These findings demonstrate that thermal stress disrupts host-microbiota homeostasis and induces oxidative and molecular responses in L. albus . This integrative response provides insight into mechanisms underlying physiological performance under thermal stress, with important implications for aquaculture sustainability.