Physiological acclimation to freshwater conditions reshapes the megalopae holobiont of Eriocheir sinensis.

Abstract

To investigate the effects of natural salinity transition on megalopae of Eriocheir sinensis, this study systematically deciphered the response and adaptation mechanisms of megalopae to low-salinity stress. The results showed that the marine-to-freshwater habitat shift significantly reshaped the intestinal microbial community structure and increased the α-diversity index. The relative abundance of core bacterial taxa such as Amaricoccus was significantly elevated, while that of the conditional pathogen Flavobacterium was significantly reduced. At the host level, natural salinity transition stress triggered a series of profound cellular and molecular responses. To eliminate damaged cells, the Caspase-mediated apoptotic pathway and the LC3-mediated autophagic pathway were significantly activated. Meanwhile, signaling pathways controlling cell proliferation and growth, including Focal adhesion, Hippo, and PI3K-Akt, were significantly inhibited. Metabolically, stress response-related pathways such as Cortisol synthesis and secretion and AMP/Adenosine signaling were activated, driving an "energy-saving" strategy characterized by enhanced catabolism and reduced anabolism of proteins and lipids. Changes in the levels of key metabolites, such as 8-hydroxyguanosine and Ectoine, further confirmed the occurrence of oxidative stress and the shift in osmotic regulation strategies. Correlation analysis revealed that the Amaricoccus was significantly correlated with key genes involved in host amino acid metabolism, oxidative stress, and the PI3K-Akt pathway, indicating that microbe-host interactions play a central role in coordinating energy redistribution to cope with osmotic stress. This study reveals the multi-dimensional adaptation mechanisms through which megalopae achieve the transition from a hyperosmotic to a hypoosmotic environment by integrating microbial community reconstruction, precise cell clearance mechanisms, and systematic metabolic reprogramming.

Abstract as supplied by the indexing source. © the authors / publisher.