Insights into the molecular mechanism of muscle textural quality improvement treated by exercise using comparative transcriptome analysis on the hybrid (Erythroculter ilishaeformis ♀ × Ancherythroculter nigrocauda ♂)

Abstract

In general, fish meat that is elastic and hard is preferred by consumers, but few methods have been identified for improving fillet quality. “Xianfeng No. 1”, a new hybrid of Erythroculter ilishaeformis (♀) × Ancherythroculter nigrocauda (♂), is an important species for aquaculture in China. A short-term exercise trial (12 days) was conducted, followed by texture and histomorphology analysis, to determine the influence of exercise on fillet hardness of this hybrid species. Furthermore, transcriptomic and bioinformatic analyses were carried out to better understand the molecular bases under the process of fillet quality formation. There are several novel findings in our study. First, exercise at a moderate velocity (1.2 body lengths per second) for 12 days can significantly increase the muscle texture (i.e., hardness and springiness) of this hybrid species. Second, the hematoxylin and eosin (H&E) staining of muscle sections indicated a decrease in myofiber diameter and increased myofiber density as the exercise duration increased. Third, a total of 2056, 2414, and 3366 differentially expressed genes (DEGs) were identified in the 4, 8, and 12 days treatment groups, respectively. Fourth, the DEGs were enriched in signaling pathways linked to muscle hardening (tight junction and hippo signaling pathways) and glucose metabolism (AMPK signaling pathways and glycolysis/gluconeogenesis). Genes associated with muscle hardening (WNT2B, CDH1, MYCB, MYH1, MYH2, and MYH6), immune defense (MAVS, EPO, and SKAP2), and glucose metabolism (HK1, GAPDH, LDHA, and PGK1) were also identified. From our study, there are several possible molecular bases on which exercise improves fillet hardness: exercise may activate hippo pathway to stimulate hyperplasia to further increase myofiber density, modulate the expression of MYHs to change myofiber type, and activate tight junction signaling pathway to narrow intermyofibrillar spaces. These findings will further accelerate the breeding of more appetizing and disease-resistant species.