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DAXX Is a Crucial Factor for Proper Development of Mammalian Oocytes and Early Embryos

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MDPI
DOI: 10.3390/ijms22031313

关键词

mammalian early development; chromatin remodeling; heterochromatin; DAXX; H3; 3 chaperones; ATRX; genome integrity

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  1. Institute of Cytology of the Russian Academy of Sciences
  2. granting program Molecular and cell biology and post-genomic technologies of the Russian Academy of Sciences

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DAXX is a multifunctional protein involved in various cellular processes, interacting with transcription factors and chromatin-remodeling proteins in the nucleus. Its specific function in mammalian early development as a chaperone of H3.3 supports proper development, impacting recruitment of ATRX and transcription of tandem repeats. Loss of DAXX results in decreased viability of early embryos.
The Death-domain associated protein 6 (DAXX) is an evolutionarily conserved and ubiquitously expressed multifunctional protein that is implicated in many cellular processes, including transcription, cellular proliferation, cell cycle regulation, Fas-induced apoptosis, and many other events. In the nucleus, DAXX interacts with transcription factors, epigenetic modifiers, and chromatin-remodeling proteins such as the transcription regulator ATRX-the alpha-thalassemia/mental retardation syndrome X-linked ATP-dependent helicase II. Accordingly, DAXX is considered one of the main players involved in chromatin silencing and one of the most important factors that maintain integrity of the genome. In this brief review, we summarize available data regarding the general and specific functions of DAXX in mammalian early development, with special emphasis on the function of DAXX as a chaperone of the histone variant H3.3. Since H3.3 plays a key role in the developmental processes, especially in the pronounced rearrangements of heterochromatin compartment during oogenesis and embryogenesis, DAXX can be considered as an important factor supporting proper development. Specifically, loss of DAXX affects the recruitment of ATRX, transcription of tandem repeats and telomere functions, which results in a decrease in the viability of early embryos.

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