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Proteome reveal abnormal spermatozoa in precocious Chinese mitten crab, Eriocheir sinensis

ABSTRACT: In juvenile Chinese mitten crabs, Eriocheir sinensis, the occurrence of sexual gland maturation in the first year is known as precocity and significantly affects culture productivity and profitability. The miniaturization of individuals is a key characteristic of precocious crabs. Most related studies focus on the underlying causes, nutritional quality, biochemical components and differentially expressed mRNAs of precocious crab individuals and tissues. The reproductive performance of precocious crabs is evaluated based on offspring quality. However, the status of precocious parental gametes (especially spermatozoa) directly related to the offspring has not been reported. To clarify the differences in spermatozoa between precocious and normal mature crabs, spermatozoal proteome data was obtained via high-throughput sequencing technology. The results revealed a total of 856 differentially expressed genes and 150 differentially expressed proteins in spermatozoa. Functional analysis showed that these genes and proteins identified in the spermatozoa of precocious E. sinensis were significantly enriched in the categories of substance and energy metabolism. And more, the miniaturization of spermatogenic cells was also identified in precocious crabs. This indicates that metabolic disorders might be the main reason for the miniaturization of spermatogenic cells in precocious E. sinensis males. The molecular defects in precocious sperm were closely related to the imbalances in essential substance and energy metabolism. These findings provide foundational information and insights into hidden biological irregularities associated with precocious phenotypes and will contribute to the further study of precocious E. sinensis males and even other crustaceans.

ORGANISM(S): Eriocheir Sinensis

SUBMITTER: Xianjiang Kang

PROVIDER: PXD037284 | iProX | Tue Oct 11 00:00:00 BST 2022

REPOSITORIES: iProX

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Project description:The global prevalence of type 2 diabetes (T2D) is increasing, and it is contributing to the susceptibility to diabetes and its related epidemic in offspring. Although the impacts of paternal T2D on metabolism of offspring have been well established, the exact molecular and mechanistic basis that mediates these impacts remains largely unclear. Here we show that paternal T2D increases the susceptibility to diabetes in offspring through the gametic epigenetic alterations. Paternal T2D led to glucose intolerance and insulin resistance in offspring. Relative to controls, offspring of T2D fathers exhibited altered gene expression patterns in the pancreatic islets, with downregulation of several genes involved in glucose metabolism and insulin signaling pathway. Epigenomic profiling of offspring pancreatic islets revealed numerous changes in cytosine methylation depending on paternal T2D, including reproducible changes in methylation over several insulin signaling genes. Paternal T2D altered overall methylome patterns in sperm, with a large portion of differentially methylated genes overlapped with that of pancreatic islets in offspring. Our study revealed, for the first time, that T2D can be inherited transgenerationally through the mammalian germline by an epigenetic manner. For all comparisons shown, male F0 founders were weaned from mothers at 3 weeks of age, and sibling males were put into cages with high-fat diet (33% energy as fat) or control diet until 12 weeks of age, at which point mice fed with HFD were injected intraperitoneally with a low dose of STZ and kept on the same diet for 4 weeks. Fasting blood glucose was examined each week post-STZ for 4 weeks, and only glucose level at 7~11 mM was considered as type 2 diabetes. Females were always raised on standard diet. At 16 weeks, male F0 founders were mated with females. After 1 or 2 days, males were removed, and pregnant females were left alone until their litters were 3 weeks of age. Note that we always used virgin females to avoid confounding effects brought about by the females. At 3 weeks of age a portion of the offspring were sacrificed and islets were generated, each from an independent father.Samples from six control and six paternal type 2 diabetes offspring were chosen for microarray analysis.

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Proteome reveal abnormal spermatozoa in precocious Chinese mitten crab, Eriocheir sinensis

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