کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5522910 1546066 2017 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
HT-2 toxin affects development of porcine parthenotes by altering DNA and histone methylation in oocytes matured in vitro
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم دامی و جانورشناسی
پیش نمایش صفحه اول مقاله
HT-2 toxin affects development of porcine parthenotes by altering DNA and histone methylation in oocytes matured in vitro
چکیده انگلیسی


- 5 mC level was increased after exposure to HT-2 toxin in porcine oocytes.
- H3K4me2 and H3K9me2 levels were increased in the oocytes from HT-2-treated group.
- HT-2 toxin treatment caused the failure of porcine parthenote development.

T-2 toxin is a type A mycotoxin produced by various Fusarium species, while HT-2 toxin is a major metabolite of T-2 toxin. Both T-2 toxin and HT-2 toxin are known to have deleterious effects on animals. Our previous work showed that HT-2 treatment caused the failure of porcine oocyte maturation. In this study, we reported that HT-2 also affected porcine embryo development. In HT-2 toxin treated group, all the percentages of embryos in 2-cell, 4-cell and blastocyst stage were significantly lower compared with those in control groups. We then explored the causes from the epigenetic modification aspect of the oocytes. The analysis of fluorescence intensity showed that 5-methyl cytosine (5 mC) level was increased after exposure to HT-2 toxin in porcine oocytes, indicating that the general DNA methylation level increased in the treated porcine oocytes. In addition, histone modifications were also affected, since our results showed that H3K4me2 and H3K9me2 levels were increased in the oocytes from HT-2-treated group. Therefore, our results indicated that HT-2 toxin decreased porcine embryo developmental competence through altering the epigenetic modifications of oocytes.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Theriogenology - Volume 103, November 2017, Pages 110-116
نویسندگان
, , , , , , ,