scholarly journals CXXC finger protein 1 is critical for T-cell intrathymic development through regulating H3K4 trimethylation

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Wenqiang Cao ◽  
Jing Guo ◽  
Xiaofeng Wen ◽  
Li Miao ◽  
Feng Lin ◽  
...  
Keyword(s):  
T Cell ◽  
H3k4 Trimethylation ◽  
Finger Protein ◽  
Cxxc Finger Protein 1

IL-7R–dependent survival and differentiation of early T-lineage progenitors is regulated by the BTB/POZ domain transcription factor Miz-1

Blood ◽  
2011 ◽  
Vol 117 (12) ◽  
pp. 3370-3381 ◽  
Author(s):  
Ingrid Saba ◽  
Christian Kosan ◽  
Lothar Vassen ◽  
Tarik Möröy
Keyword(s):  
T Cells ◽  
Transcription Factor ◽  
T Cell ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Strong Reduction ◽  
Expression Levels ◽  
Cell Numbers ◽  
Finger Protein

Abstract T cells originate from early T lineage precursors that have entered the thymus and differentiate through well-defined steps. Mice deficient for the BTB/POZ domain of zinc finger protein-1 (Miz-1) almost entirely lack early T lineage precursors and have a CD4−CD8− to CD4+CD8+ block causing a strong reduction in thymic cellularity. Miz-1ΔPOZ pro-T cells cannot differentiate in vitro and are unable to relay signals from the interleukin-7R (IL-7R). Both STAT5 phosphorylation and Bcl-2 up-regulation are perturbed. The high expression levels of SOCS1 found in Miz-1ΔPOZ cells probably cause these alterations. Moreover, Miz-1 can bind to the SOCS1 promoter, suggesting that Miz-1 deficiency causes a deregulation of SOCS1. Transgenic overexpression of Bcl-2 or inhibition of SOCS1 restored pro-T cell numbers and their ability to differentiate, supporting the hypothesis that Miz-1 is required for the regulation of the IL-7/IL-7R/STAT5/Bcl-2 signaling pathway by monitoring the expression levels of SOCS1.

scholarly journals Role of CxxC-finger protein 1 in establishing mouse oocyte epigenetic landscapes

2021 ◽  
Author(s):  
Qian-Qian Sha ◽  
Ye-Zhang Zhu ◽  
Yunlong Xiang ◽  
Jia-Li Yu ◽  
Xiao-Ying Fan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Histone H3 ◽  
Finger Protein ◽  
Maternal Genome ◽  
Wide Range ◽  
Transcriptional Changes ◽  
Nuclear Events ◽  
Genomic Regions ◽  
Cxxc Finger Protein 1

Abstract During oogenesis, oocytes gain competence and subsequently undergo meiotic maturation and prepare for embryonic development; trimethylated histone H3 on lysine-4 (H3K4me3) mediates a wide range of nuclear events during these processes. Oocyte-specific knockout of CxxC-finger protein 1 (CXXC1, also known as CFP1) impairs H3K4me3 accumulation and causes changes in chromatin configurations. This study investigated the changes in genomic H3K4me3 landscapes in oocytes with Cxxc1 knockout and the effects on other epigenetic factors such as the DNA methylation, H3K27me3, H2AK119ub1 and H3K36me3. H3K4me3 is overall decreased after knocking out Cxxc1, including both the promoter region and the gene body. CXXC1 and MLL2, which is another histone H3 methyltransferase, have nonoverlapping roles in mediating H3K4 trimethylation during oogenesis. Cxxc1 deletion caused a decrease in DNA methylation levels and affected H3K27me3 and H2AK119ub1 distributions, particularly at regions with high DNA methylation levels. The changes in epigenetic networks implicated by Cxxc1 deletion were correlated with the transcriptional changes in genes in the corresponding genomic regions. This study elucidates the epigenetic changes underlying the phenotypes and molecular defects in oocytes with deleted Cxxc1 and highlights the role of CXXC1 in orchestrating multiple factors that are involved in establishing the appropriate epigenetic states of maternal genome.

The zinc finger protein cKrox directs CD4 lineage differentiation during intrathymic T cell positive selection

2005 ◽  
Vol 6 (4) ◽  
pp. 373-381 ◽  
Author(s):  
Guangping Sun ◽  
Xiaolong Liu ◽  
Peter Mercado ◽  
S Rhiannon Jenkinson ◽  
Magdalini Kypriotou ◽  
...  
Keyword(s):  
T Cell ◽  
Positive Selection ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Lineage Differentiation ◽  
Finger Protein

scholarly journals CXXC finger protein 1-mediated histone H3 lysine-4 trimethylation is essential for proper meiotic crossover formation in mice

Development ◽  
2020 ◽  
Vol 147 (6) ◽  
pp. dev183764 ◽  
Author(s):  
Yu Jiang ◽  
Hui-Ying Zhang ◽  
Zhen Lin ◽  
Ye-Zhang Zhu ◽  
Chao Yu ◽  
...  
Keyword(s):  
Histone H3 ◽  
Finger Protein ◽  
Meiotic Crossover ◽  
Cxxc Finger Protein 1

scholarly journals Zinc finger protein Zfp335 is required for the formation of the naïve T cell compartment

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Brenda Y Han ◽  
Shuang Wu ◽  
Chuan-Sheng Foo ◽  
Robert M Horton ◽  
Craig N Jenne ◽  
...  
Keyword(s):  
T Cell ◽  
Zinc Finger ◽  
Target Genes ◽  
Zinc Finger Protein ◽  
Cell Maturation ◽  
Developmental Defect ◽  
Finger Protein ◽  
T Cell Maturation ◽  
Naïve T Cell ◽  
Naive T Cell

The generation of naïve T lymphocytes is critical for immune function yet the mechanisms governing their maturation remain incompletely understood. We have identified a mouse mutant, bloto, that harbors a hypomorphic mutation in the zinc finger protein Zfp335. Zfp335bloto/bloto mice exhibit a naïve T cell deficiency due to an intrinsic developmental defect that begins to manifest in the thymus and continues into the periphery, affecting T cells that have recently undergone thymic egress. The effects of Zfp335bloto are multigenic and cannot be attributed to altered thymic selection, proliferation or Bcl2-dependent survival. Zfp335 binds to promoter regions via a consensus motif, and its target genes are enriched in categories related to protein metabolism, mitochondrial function, and transcriptional regulation. Restoring the expression of one target, Ankle2, partially rescues T cell maturation. These findings identify Zfp335 as a transcription factor and essential regulator of late-stage intrathymic and post-thymic T cell maturation.

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