Pythium porphyrae?and?P. chondricola, collectively known as the red-rot pathogens, pose a severe threat to nori （Pyropia/Porphyra） cultivation, causing substantial economic losses globally. A critical factor underpinning their success as pathogens is their remarkable resilience and adaptability to fluctuating environmental conditions, enabling persistent survival and infection. While investigating the genomic basis of this adaptability, we identified a significant expansion of the?EctC?gene, which encodes a key enzyme, ectoine synthase, in the biosynthesis pathway of the compatible solute ectoine （1,4,5,6-tetrahydro-2-methyl-4-pyrimidine carboxylic acid）. Ectoine is a potent stress-protectant molecule, well-characterized in prokaryotes for its role in osmoprotection and stabilization of macromolecules under various abiotic stresses, including high salinity, drought, temperature extremes, and oxidative stress. Its confirmed presence and potential functional role in eukaryotic oomycetes, particularly in plant pathogens, represents a paradigm shift, as it was historically considered a prokaryotic-specific metabolite. This study aimed to functionally characterize the role of the?EctC?gene from?P. porphyrae?（PpEctC） in the context of oomycete growth, environmental stress tolerance, and pathogenicity. We employed a heterologous functional genomics approach using the established?Phytophthora sojae?transformation system. We generated a comprehensive set of transgenic strains in?P. sojae?strain P6497 to dissect the function of?EctC. Using a CRISPR/Cas9-mediated gene replacement strategy coupled with Homology-Directed Repair （HDR）, we successfully created a?PsEctC?knockout mutant （PsΔEctC-RFP）, where the native?PsEctC?gene was replaced with a Red Fluorescent Protein （RFP） marker. Furthermore, we generated a heterologous complementation strain （PsΔEctC-PpEctC） by replacing?PsEctC?with the?PpEctC?gene from?P. porphyrae. Additionally, we constructed overexpression （Ps-oeEctC, overexpressing?PsEctC） and heterologous expression （Ps-hePpEctC, expressing?PpEctC?in the wild-type?P. sojae?background） strains using plasmid-based expression systems. All transgenic strains were rigorously validated through PCR, qRT-PCR, and phenotypic screening to confirm successful gene editing, deletion, and altered expression levels. Phenotypic characterization under standard conditions revealed that the deletion of?PsEctC?significantly impaired mycelial growth, as evidenced by the significantly smaller colony diameter of the PsΔEctC-RFP mutant compared to the wild-type （WT） and empty vector control （CK）. Intriguingly, heterologous complementation with?PpEctC?in the PsΔEctC-PpEctC strain fully restored mycelial growth to WT levels, demonstrating the functional equivalence and cross-species compatibility of the?P. porphyrae?gene in supporting basic vegetative growth. In contrast, neither the knockout nor the complementation significantly affected sporangia formation or zoospore production, except for an unexplained reduction in zoospore yield in the PsΔEctC-PpEctC, suggesting that?EctC?is primarily involved in hyphal expansion but not in these specific developmental reproductive stages under non-stress conditions. The core of our investigation focused on the role of?EctC?in stress tolerance. Under high salinity stress （35‰ NaCl）, the PsΔEctC-RFP knockout mutant exhibited a dramatic reduction in relative growth, highlighting its heightened sensitivity to osmotic stress. The heterologous complementation strain （PsΔEctC-PpEctC） displayed a growth tolerance phenotype statistically indistinguishable from the WT and CK, confirming that?PpEctC?can effectively restore osmotolerance. Strikingly, both the?PsEctC?overexpression （Ps-oeEctC） and?PpEctC?heterologous expression （Ps-hePpEctC） demonstrated superior growth under high salt conditions, significantly outperforming the WT. This indicates that elevated?EctC?expression, whether from the native or a heterologous source, confers a distinct advantage under osmotic duress. A similar trend was observed under alkaline pH stress （pH 9）, where the?EctC?knockout mutant was severely compromised, while the complemented and overexpression mutants maintained robust growth, underscoring ectoine's role in pH stress mitigation. Given the critical role of Reactive Oxygen Species （ROS） in plant defense, we assessed the total antioxidant capacity of the transformants. The results were highly consistent: the PsΔEctC-RFP mutant showed a significant decrease in antioxidant capability. Conversely, both the Ps-oeEctC and Ps-hePpEctC mutants exhibited a substantial enhancement in their antioxidant capacity, with the latter showing the most potent effect. The complementation strain （PsΔEctC-PpEctC） showed a partial but significant recovery in antioxidant capacity compared to the knockout, though it did not reach WT levels. This establishes a clear link between?EctC-mediated ectoine synthesis and the augmentation of the pathogen's oxidative stress defense system, a crucial attribute for countering host-induced oxidative bursts during infection. Pathogenicity assays on etiolated soybean hypocotyls provided compelling evidence for the role of?EctC?in virulence. The PsΔEctC-RFP knockout strain caused minimal lesions and showed a significantly lower relative in planta biomass compared to the WT, indicating severely attenuated virulence. Complementation with?PpEctC?（PsΔEctC-PpEctC） partially restored pathogenicity, leading to higher biomass than the knockout, though not fully to WT levels. Most notably, the heterologous expression of?PpEctC?（Ps-hePpEctC） resulted in hyper-virulence, with a significantly greater pathogen biomass recovered from infected tissues compared to the WT. The overexpression mutant （Ps-oeEctC） also showed enhanced virulence compared to the WT. These findings strongly suggest that?EctC?is a critical virulence factor, and its enhanced expression can potentiate the pathogen's infectivity and colonization ability, likely through bolstered resistance to host-imposed environmental and oxidative stresses. In conclusion, our study provides comprehensive functional evidence that the ectoine synthase gene?EctC, particularly the?PpEctC?variant from?P. porphyrae, plays a multifaceted and pivotal role in oomycete biology. It is integral for optimal mycelial growth, essential for tolerance to high salinity and alkaline pH, crucial for enhancing antioxidant capacity, and is a significant determinant of pathogenicity. The successful heterologous complementation and the hyper-virulent phenotype induced by heterologous expression confirm the functional potency of?PpEctC. This research not only elucidates a previously uncharacterized stress adaptation mechanism in a destructive eukaryotic pathogen but also pinpoints?EctC?and the ectoine biosynthesis pathway as a promising and novel target for developing precise disease control strategies against red-rot disease in nori aquaculture. Future work will focus on validating these findings directly in?P. porphyrae?upon the establishment of a robust transformation system.