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Isoform-specific imprinting of the MEST gene in porcine parthenogenetic fetuses. | LitMetric

Isoform-specific imprinting of the MEST gene in porcine parthenogenetic fetuses.

Gene

Jilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Science, Jilin University, Changchun 130062, China. Electronic address:

Published: March 2015

AI Article Synopsis

  • The study focuses on the role of the MEST gene, an important maternally imprinted gene, in the development of parthenogenetic fetuses in pigs, highlighting its significance in embryonic growth and potential links to cancer.
  • Researchers identified three isoforms of porcine MEST and examined their mRNA expression and methylation levels in both parthenogenetic and control fetuses using advanced genetic analysis techniques.
  • Findings revealed that while MEST-1A and MEST-1B were expressed similarly in both groups, MEST-1C showed no expression in parthenogenetic fetuses, suggesting that its differential methylation may play a critical role in developmental issues associated with abnormal gene imprinting.

Article Abstract

Aberrant expression of imprinted genes is the main reason for developmental retardation in mammalian parthenogenetic fetuses. Mesoderm specific transcript (MEST) is a maternally imprinted gene that is linked to cancer and is necessary for normal early embryonic development. Tissue and isoform-specific imprinting of MEST have been identified in humans and mice, but have not yet been identified in pigs. In this study, the three isoforms of porcine MEST were identified using the GenBank and Ensembl sequence databases. Then, we determined MEST isoform-specific mRNA expression and methylation levels by quantitative real-time PCR (qRT-PCR) and bisulfite sequencing PCR analysis (BSP) between porcine parthenogenetic (PA) and control (Con) fetuses, respectively. Altogether, our results demonstrated that the expression of MEST-1A and MEST-1B has no evident differences between PA and Con groups; however, there is no expression of MEST-1C in PA fetuses. In addition, the results of BSP showed that the hypermethylation of exon 1c of MEST-1C was observed in PA samples. Thus, we suggested that MEST-1C was isoform-specific imprinting, which may be contributed to differential methylation status of exon 1c in porcine fetuses.

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Source
http://dx.doi.org/10.1016/j.gene.2015.01.031DOI Listing

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