The mismatch between the rapid expansion of breeding scale and outdated techniques has hindered the development of the sea cucumber (A. japonicus) industry. Our previous work revealed that ecological seedling breeding can produce red-colored A. japonicus, a phenotype not observed in traditional artificial breeding, where individuals are typically green. To investigate the molecular and genetic basis of this novel red coloration, we compared the growth conditions of red sea cucumbers and green sea cucumbers, as well as the differences in the pigment composition, gene expression and metabolites of their body walls. Red individuals showed higher body length and weight, and elevated levels of astaxanthin, lutein, canthaxanthin, and β-carotene in the body wall. Transcriptomic and metabolomic analyses identified differentially expressed genes and metabolites associated with pigmentation. In particular, FMO2 and WDR18, involved in the cytochrome P450 drug metabolism pathway, were significantly upregulated in red individuals and are known to play roles in pigment biosynthesis and light signal perception. Key metabolites such as astaxanthin and fucoxanthin were implicated in body color formation. Moreover, genes in the arachidonic acid metabolism pathway were highly expressed, suggesting that dietary factors may contribute to pigment synthesis and accumulation. These findings provide novel insights into the mechanisms underlying body color variation in A. japonicus and offer potential for improved breeding strategies.

Extreme weather events such as heavy rainfall significantly reduce surface salinity in coastal waters, presenting considerable challenges to the aquaculture of Japanese scallops (Mizuhopecten yessoensis) in shallow cage systems. This study investigated the effects of chronic low-salinity stress on the growth performance, antioxidant capacity, and gene expression profile of M. yessoensis using a 60-day salinity gradient experiment. S33 represents the control treatment with normal seawater salinity (33‰), while S30, S28, and S26 represent experimental groups with progressively lower salinities of 30‰, 28‰, and 26‰, respectively. A decline in salinity was accompanied by an increase in oxygen consumption. The S26 group exhibited a higher ammonia excretion rate (2.73 μg/g·h) than other groups, indicating intensified nitrogen metabolism. Growth was inhibited under low-salinity conditions. The S33 group exhibited greater weight gain (16.7%) and shell growth (8.4%) compared to the S26 group (11.6% and 6%), which also showed a substantially higher mortality rate (46%) compared to the control (13%). At 28‰, antioxidant enzyme activities (T-AOC, SOD, CAT, POD) were elevated, indicating a moderate level of stress. However, at the lowest salinity (26‰), these indicators decreased, reflecting the exhaustion of the antioxidant systems and indicating that the mollusks’ adaptive capacity had been exceeded, leading to a state of stress fatigue. NAD-MDH activity was elevated in the S26 group, reflecting enhanced aerobic metabolism under stress. Transcriptome analysis revealed 564 differentially expressed genes (DEGs) between the S33 and S26 groups. Functional enrichment analysis indicated that these DEGs were mainly associated with immune and stress response pathways, including NF-κB, TNF, apoptosis, and Toll/Imd signaling. These genes are involved in key metabolic processes, such as alanine, aspartate, and glutamate metabolism. Genes such as GADD45, ATF4, TRAF3, and XBP1 were upregulated, contributing to stress repair and antioxidant responses. Conversely, the expressions of CASP3, IKBKA, BIRC2/3, and LBP were downregulated, potentially mitigating apoptosis and inflammatory responses. These findings suggest that M. yessoensis adapts to chronic low-salinity stress through the activation of antioxidant systems, modulation of immune responses, and suppression of excessive apoptosis. This study provides new insights into the molecular mechanisms underlying salinity adaptation in bivalves and offers valuable references for scallop aquaculture and selective breeding programs.

This review aims to advance the development of biofloc technology (BFT), providing more sustainable and efficient practices for the farming of the Japanese sea cucumber (Apostichopus japonicus). BFT is a sustainable aquaculture method that promotes nutrient recycling and effective carbon source management, offering significant advantages such as improving water quality, enhancing growth performance, and boosting the physiological activity and disease resistance of cultured animals. In A. japonicus farming, the optimal carbon source is glucose, and the ideal carbon-to-nitrogen (C/N) ratio ranges between 15 and 20. Microbial additives, such as the Bacillus species, have been shown to enhance biofloc formation and growth, as well as the immune responses in A. japonicus. However, the technology also faces limitations, including finding suitable biofloc culture protocols that match the physiological habits of A. japonicus and potential challenges with biofloc stability under varying environmental conditions. Based on existing research, this review discusses these limitations in the farming of A. japonicus. Additionally, it compares biofloc farming models for other economically important aquatic species. By addressing these key aspects, this review offers insights to enhance BFT performance, ultimately contributing to more efficient and sustainable A. japonicus aquaculture practices.

The sea cucumber (Apostichopus japonicus) is highly susceptible to environmental stress during aquaculture, storage, and transportation, often resulting in autolysis and considerable economic losses. UVA irradiation and Vibrio splendidus infection were used to induce skin ulceration in A. japonicus. In this study, UVA irradiation and V. splendidus infection were used to induce skin ulceration, and the effectiveness of a compound inhibitor in delaying its onset was evaluated. The degree of skin ulceration in A. japonicus was evaluated. Body wall tissues were collected to measure the activities of self-digesting enzymes, AchE, cathepsin L, SOD, and CAT. Caspase-3 expression was also analyzed to assess apoptosis and tissue damage. The results indicated that soaking A. japonicus in the inhibitor composition significantly delayed the onset of skin ulceration. After 72 h of UVA irradiation, the skin ulceration in group Eg was 0.55%, which was significantly lower than that in groups Cg and Wg. In the V. splendidus infection model, group Eg showed a 4-day delay in the onset of skin ulceration, compared to group Cg. Enzyme activity and gene expression analysis revealed that the inhibitor composition significantly reduced self-digesting enzyme expression in the A. japonicus body wall, increased SOD and CAT activities, and inhibited Caspase-3 expression. This study provides valuable theoretical insights into controlling skin ulceration in A. japonicus during aquaculture, preservation, and transportation.

Sea urchin aquaculture has experienced remarkable growth in recent years. However, this growth has been accompanied by increased disease prevalence. Notably, spotting disease has particularly severe impacts. In this study, we isolated the pathogen HZ-3-2 from 10 sea urchins with spotting disease, and it was identified as Vibrio splendidus through morphological observations, 16S rDNA sequencing, and whole-genome sequencing. Subsequently, experimental infection confirmed that V. splendidus (HZ-3-2) is the causative agent of spotting disease in this outbreak. The drug sensitivity confirmed the presence of drug resistance genes, such as CPR, QNRS5, and rsmA, which were identified in the genome. The tests indicated that V. splendidus was sensitive to various antibiotics, including fluoroquinolones and florfenicol. Finally, we used the transcriptome to explore the molecular response of the diseased sea urchin. Compared to the control group, a group of sea urchins immersed in a pathogen suspension with a concentration of 10⁷ CFU/mL (group M) resulted in 439 annotated differentially expressed genes. KEGG pathway analysis indicated significant activation of cholesterol metabolism and starch and sucrose metabolism in the S. intermedius. This study highlights the genes NPC1, AMY2A, and MGAM as critical regulators of energy metabolism, and cholesterol synthesis in infected sea urchins. These findings confirm V. splendidus as the bacterium responsible for spotting disease and provide valuable insights into the intestinal molecular response of S. intermedius to infection.

The histological integrity of the intestine depends on the tight and orderly arrangement of epithelial cells within the intestinal villi. Nodal, a transforming growth factor-β (TGF-β) family member, has been reported to promote epithelial cell proliferation. Collagen not only establishes physical connections between adjacent cells but also serves as an anchoring platform for cell adhesion and regeneration processes. Therefore, a 21-day feeding trial was conducted using RNA interference to investigate the role of the Nodal gene in regulating intestinal collagen synthesis and histological structure integrity in juvenile A. japonicus fed diets containing graded levels of vitamin E (VE) (0, 200, and 400 mg/kg). The results showed that the addition of 200 mg/kg VE significantly improved the growth rate, immune enzyme activities and related gene expression, as well as intestinal villus morphology. Additionally, the addition of 200 mg/kg VE upregulated the expression of Nodal, which activated the expression of collagen synthesis-related genes and promoted collagen deposition in the intestines of A. japonicus. After Nodal gene knockdown, A. japonicus presented a decreased growth rate, damage to the intestinal histological structure, and impaired collagen synthesis, with the most notable findings observed in A. japonicus fed diets without VE addition. However, these detrimental effects were eliminated to some extent by the addition of 200 mg/kg VE. These findings indicate that VE improves immune function and intestinal histological structure in A. japonicus through a Nodal-dependent pathway.