4.7 Article

Transcriptome and Network Analyses Reveal the Gene Set Involved in PST Accumulation and Responses to Toxic Alexandrium minutum Exposure in the Gills of Chlamys farreri

期刊

出版社

MDPI
DOI: 10.3390/ijms23147912

关键词

paralytic shellfish toxins; Zhikong scallop; gills; weighted gene co-expression network; OCTN1s

资金

  1. National Key R&D Program of China [2018YFD0900604]
  2. National Natural Science Foundation of China [31802292]
  3. Taishan Industry Leading Talent Project [LJNY201816]
  4. Sanya Yazhou Bay Science and Technology City [SKJC-KJ-2019KY01]

向作者/读者索取更多资源

This study provides insights into the molecular mechanism of bivalve resistance to paralytic shellfish toxins (PST) by examining the gene set involved in PST accumulation in scallop gills. Transcriptomic analysis revealed different response mechanisms of scallop to PST-producing dinoflagellate at different stages of exposure. The study also found that PST exposure affects nervous system development, xenobiotic metabolism, substance transport, and immune functions, ultimately leading to apoptosis.
Bivalve molluscs are filter-feeding organisms that can accumulate paralytic shellfish toxins (PST) through ingesting toxic marine dinoflagellates. While the effects of PST accumulation upon the physiology of bivalves have been documented, the underlying molecular mechanism remains poorly understood. In this study, transcriptomic analysis was performed in the gills of Zhikong scallop (Chlamys farreri) after 1, 3, 5, 10, and 15 day(s) exposure of PST-producing dinoflagellate Alexandrium minutum. Higher numbers of differentially expressed genes (DEGs) were detected at day 1 (1538) and day 15 (989) than that at day 3 (77), day 5 (82), and day 10 (80) after exposure, and most of the DEGs were only regulated at day 1 or day 15, highlighting different response mechanisms of scallop to PST-producing dinoflagellate at different stages of exposure. Functional enrichment results suggested that PST exposure induced the alterations of nervous system development processes and the activation of xenobiotic metabolism and substance transport processes at the acute and chronic stages of exposure, respectively, while the immune functions were inhibited by PST and might ultimately cause the activation of apoptosis. Furthermore, a weighted gene co-expression network was constructed, and ten responsive modules for toxic algae exposure were identified, among which the yellow module was found to be significantly correlated with PST content. Most of the hub genes in the yellow module were annotated as solute carriers (SLCs) with eight being OCTN1s, implying their dominant roles in regulating PST accumulation in scallop gills. Overall, our results reveal the gene set responding to and involved in PST accumulation in scallop gills, which will deepen our understanding of the molecular mechanism of bivalve resistance to PST.

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