scholarly journals Beta-Oxidation Is Essential for Mouse Oocyte Developmental Competence and Early Embryo Development1

2010 ◽  
Vol 83 (6) ◽  
pp. 909-918 ◽  
Author(s):  
Kylie R. Dunning ◽  
Kara Cashman ◽  
Darryl L. Russell ◽  
Jeremy G. Thompson ◽  
Robert J. Norman ◽  
...  
2010 ◽  
Vol 83 (Suppl_1) ◽  
pp. 154-154
Author(s):  
Kylie R. Dunning ◽  
Kara Cashman ◽  
Darryl L. Russell ◽  
Jeremy Thompson ◽  
Robert Norman ◽  
...  

2014 ◽  
Vol 20 (4) ◽  
pp. 1158-1166 ◽  
Author(s):  
Cheng-Cheng Zhu ◽  
Yan-Jun Hou ◽  
Jun Han ◽  
Hong-Lin Liu ◽  
Xiang-Shun Cui ◽  
...  

AbstractMycotoxins, such as aflatoxin (AF), fumonisin B1, zearalenone (ZEA), and deoxynivalenol (DON), are commonly found in many food commodities. Mycotoxins have been shown to increase DNA methylation levels in a human intestinal cell line. We previously showed that the developmental competence of oocytes was affected in mice that had been fed a mycotoxin-containing diet. In this study, we explored possible mechanisms of low mouse oocyte developmental competence after mycotoxin treatment in an epigenetic modification perspective. Mycotoxin-contaminated maize (DON at 3,875μg/kg, ZEA at 1,897μg/kg, and AF at 806μg/kg) was included in diets at three different doses (mass percentage: 0, 15, and 30%) and fed to mice for 4 weeks. The fluorescence intensity analysis showed that the general DNA methylation levels increased in oocytes from high dose mycotoxin-fed mice. Mouse oocyte histone methylation was also altered. H3K9me3 and H4K20me3 level increased in oocytes from mycotoxin-fed mice, whereas H3K27me3 and H4K20me2 level decreased in oocytes from mycotoxin-fed mice. Thus, our results indicate that naturally occurring mycotoxins have effects on epigenetic modifications in mouse oocytes, which may be one of the reasons for reduced oocyte developmental competence.


2020 ◽  
Author(s):  
Rowena Smith ◽  
Zongliang Jiang ◽  
Andrej Susor ◽  
Hao Ming ◽  
Janet Tait ◽  
...  

AbstractReproductive success relies on a healthy oocyte competent for fertilisation and capable of sustaining early embryo development. By the end of oogenesis, the oocyte is characterised by a transcriptionally silenced state, but the significance of this state and how it is achieved remains poorly understood. Histone H3.3, one of the H3 variants, has unique functions in chromatin structure and gene expression that are cell cycle-independent. We report here a comprehensive characterisation of the roles of the subunits of the Hira complex (i.e. Hira, Cabin1 and Ubn1), which is primarily responsible for H3.3 deposition during mouse oocyte development. Loss-of-function of any component of the Hira complex led to early embryogenesis failure. Transcriptome and nascent RNA analyses revealed that mutant oocytes fail to silence global transcription. Hira complex mutants are unable to establish the H3K4me3 and H3K9me3 repressive marks, resulting in aberrant chromatin accessibility. Among the misregulated genes in mutant oocytes is Zscan4, a 2-cell specific gene that is involved in zygote genome activation. Overexpression of Zscan4 recapitulates the phenotypes of Hira mutants, illustrating that temporal and spatial expression of Zscan4 is fine-tuned at the oocyte-to-embryo transition. Thus, the H3.3 chaperone Hira complex has a maternal effect function in oocyte developmental competence and early embryogenesis by modulating chromatin condensation and transcriptional quiescence.


Cryobiology ◽  
2021 ◽  
Vol 103 ◽  
pp. 186
Author(s):  
Akshatha Daddangadi ◽  
Shubhashree Uppangala ◽  
Satish Kumar Adiga

Sign in / Sign up

Export Citation Format

Share Document