Histone H2A.X phosphorylation and Caspase-Initiated Chromatin Condensation in late-stage erythropoiesis

Jeffery, Nazish N.; Davidson, Christina; Peslak, Scott A.; Kingsley, Paul D.; Nakamura, Yukio; Palis, James; Bulger, Michael

doi:10.1186/s13072-021-00408-5

Cited by 12 publications

(6 citation statements)

References 54 publications

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“…H2AX knock-out mice show macrocytic anemia and dysregulation of the gene programs associated with late erythroid maturation. A larger proportion of the population are immature erythroblasts with an increased nuclear:cytoplasmic ratio [84]. These cells accumulate less hemoglobin in the first 4 days of maturation and cannot condense their nuclei compared to WT cells.…”

Section: Phosphorylated Tyr142mentioning

confidence: 99%

BAZ1B the Protean Protein

Sharif

Zamani

Chadwick

2021

Genes

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The bromodomain adjacent to the zinc finger domain 1B (BAZ1B) or Williams syndrome transcription factor (WSTF) are just two of the names referring the same protein that is encoded by the WBSCR9 gene and is among the 26–28 genes that are lost from one copy of 7q11.23 in Williams syndrome (WS: OMIM 194050). Patients afflicted by this contiguous gene deletion disorder present with a range of symptoms including cardiovascular complications, developmental defects as well as a characteristic cognitive and behavioral profile. Studies in patients with atypical deletions and mouse models support BAZ1B hemizygosity as a contributing factor to some of the phenotypes. Focused analysis on BAZ1B has revealed this to be a versatile nuclear protein with a central role in chromatin remodeling through two distinct complexes as well as being involved in the replication and repair of DNA, transcriptional processes involving RNA Polymerases I, II, and III as well as possessing kinase activity. Here, we provide a comprehensive review to summarize the many aspects of BAZ1B function including its recent link to cancer.

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Section: Phosphorylated Tyr142mentioning

confidence: 99%

BAZ1B the Protean Protein

Sharif

Zamani

Chadwick

2021

Genes

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“…[97][98][99] Histone phosphorylation usually occurs at H3 or H2A of serine, threonine, and tyrosine, which is related to centromere function, chromosome condensation, and transcriptional activation. [100][101][102] Histone lysine β-hydroxybutyrylation (Kbhb) was first reported in 2016, whose levels were significantly elevated under conditions of diabetic ketosis or starvation. 103 Kbhb is catalysed by p300, while SIRT1 to SIRT3 and HDAC1 to HDAC3 remove Kbhb.…”

Section: Epigenetic Regulatory Mechanismsmentioning

confidence: 99%

Epigenetic regulation in metabolic diseases: mechanisms and advances in clinical study

Lin

et al. 2023

Sig Transduct Target Ther

134

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Epigenetics regulates gene expression and has been confirmed to play a critical role in a variety of metabolic diseases, such as diabetes, obesity, non-alcoholic fatty liver disease (NAFLD), osteoporosis, gout, hyperthyroidism, hypothyroidism and others. The term ‘epigenetics’ was firstly proposed in 1942 and with the development of technologies, the exploration of epigenetics has made great progresses. There are four main epigenetic mechanisms, including DNA methylation, histone modification, chromatin remodelling, and noncoding RNA (ncRNA), which exert different effects on metabolic diseases. Genetic and non-genetic factors, including ageing, diet, and exercise, interact with epigenetics and jointly affect the formation of a phenotype. Understanding epigenetics could be applied to diagnosing and treating metabolic diseases in the clinic, including epigenetic biomarkers, epigenetic drugs, and epigenetic editing. In this review, we introduce the brief history of epigenetics as well as the milestone events since the proposal of the term ‘epigenetics’. Moreover, we summarise the research methods of epigenetics and introduce four main general mechanisms of epigenetic modulation. Furthermore, we summarise epigenetic mechanisms in metabolic diseases and introduce the interaction between epigenetics and genetic or non-genetic factors. Finally, we introduce the clinical trials and applications of epigenetics in metabolic diseases.

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“…Given the physiological significance of enucleation in generating highly deformable RBCs for effective oxygen delivery, understanding the mechanistic basis of enucleation has been an active area of investigation. Cytoskeleton proteins such as actin ( Takano-Ohmuro et al, 1996 ; Ji et al, 2008 ; Watanabe et al, 2013 ; Ubukawa et al, 2020 ; Liu et al, 2021 ), tubulin ( Chasis et al, 1989 ; Wang et al, 2012 ), myosin ( Takano-Ohmuro et al, 1996 ; Ubukawa et al, 2012 ), tropomodulin ( Sui et al, 2014 ), and chromatin condensation and lipid rafts ( Ji et al, 2010 ; Konstantinidis et al, 2012 ; Malik et al, 2017 ; Zhao et al, 2019 ; Wang et al, 2021 ; Jeffery et al, 2021 ) are essential for normal enucleation. Although the function of actin and tubulin in enucleation suggests that erythroblast enucleation is a form of asymmetric cytokinesis, evidence documents that vesicle trafficking rather than cytokinesis is required for enucleation ( Keerthivasan et al, 2010 ).…”

Section: Normal Erythropoiesismentioning

confidence: 99%

Normal and dysregulated crosstalk between iron metabolism and erythropoiesis

Ginzburg

Rivella

et al. 2023

eLife

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Erythroblasts possess unique characteristics as they undergo differentiation from hematopoietic stem cells. During terminal erythropoiesis, these cells incorporate large amounts of iron in order to generate hemoglobin and ultimately undergo enucleation to become mature red blood cells, ultimately delivering oxygen in the circulation. Thus, erythropoiesis is a finely tuned, multifaceted process requiring numerous properly timed physiological events to maintain efficient production of 2 million red blood cells per second in steady state. Iron is required for normal functioning in all human cells, the erythropoietic compartment consuming the majority in light of the high iron requirements for hemoglobin synthesis. Recent evidence regarding the crosstalk between erythropoiesis and iron metabolism sheds light on the regulation of iron availability by erythroblasts and the consequences of insufficient as well as excess iron on erythroid lineage proliferation and differentiation. In addition, significant progress has been made in our understanding of dysregulated iron metabolism in various congenital and acquired malignant and non-malignant diseases. Finally, we report several actual as well as theoretical opportunities for translating the recently acquired robust mechanistic understanding of iron metabolism regulation to improve management of patients with disordered erythropoiesis, such as anemia of chronic inflammation, β-thalassemia, polycythemia vera, and myelodysplastic syndromes.

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Histone H2A.X phosphorylation and Caspase-Initiated Chromatin Condensation in late-stage erythropoiesis

Cited by 12 publications

References 54 publications

BAZ1B the Protean Protein

BAZ1B the Protean Protein

Epigenetic regulation in metabolic diseases: mechanisms and advances in clinical study

Normal and dysregulated crosstalk between iron metabolism and erythropoiesis

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