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Cell fate decision by a morphogen-transcription factor-chromatin modifier axis

ABSTRACT: The IP-MS data includes SALL4 IP-MS data with or without BMP4 treatment at day 3 of JGES reprogramming, each group contain 3 repeats.

ORGANISM(S): Mus Musculus

SUBMITTER: Duanqing Pei

PROVIDER: PXD051433 | iProX | Fri Apr 12 00:00:00 BST 2024

REPOSITORIES: iProX

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Cell fate decision by a morphogen-transcription factor-chromatin modifier axis.

Ming Jin J Lin Lihui L Li Jiajun J Wu Linlin L Fang Shicai S Huang Tao T Fu Yu Y Liu Dong D Zhang Wenhui W Li Chen C Yang Yongzheng Y Huang Yi Y Qin Yue Y Kuang Junqi J Huang Xingnan X Guo Liman L Zhang Xiaofei X Liu Jing J Chen Jiekai J Zhao Chengchen C Wang Bo B Pei Duanqing D

Nature communications 20240729 1

Cell fate decisions remain poorly understood at the molecular level. Embryogenesis provides a unique opportunity to analyze molecular details associated with cell fate decisions. Works based on model organisms have provided a conceptual framework of genes that specify cell fate control, for example, transcription factors (TFs) controlling processes from pluripotency to immunity<sup>1</sup>. How TFs specify cell fate remains poorly understood. Here we report that SALL4 relies on NuRD (nucleosome- ...[more]

PMID: 39075094

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Cell fate decision by a morphogen-transcription factor-chromatin modifier axis

Project description:Bulk RNA-sequences show the differences upon primitive endoderm cell related gene expression between JGES induced somatic cell reprogramming with or without BMP4 treatment, and between WT-SALL4 or delN12-SALL4 induced transdifferentiation from E13.5 mouse embryonic fibroblasts, primitive endoderm cell related gene are from our single cell RNA sequence data So as to estimate the chromatin remodeling differences between SALL4-WT and SALL4-delN12 during single factor induced PrE formation, we performed Tn5 dependent ATAC-sequence to compare the open and close chromatin of the two group. In order to identify the bingding differences of SALL4 and H3K27ac level diversity between SALL4-WT and SALL4-delN12 on PrE related genes, wo performed CUTandTAG experiments. Single cell analysis provides clarity unattainable with bulk approaches. Here we apply single cell RNA-seq to a newly established mouse somatic cell reprogramming system with or without BMP4 treatment at Day 7, this reprogramming system are induced by four transcriptional factors Jdp2-Glis1-Esrrb-Sall4 or JGES and cultured in iCD3. We first show that cells could be clustered into four group, primitive endoderm cell like cells, pluripotent cells, endothelial cells, and intermediate state cells which are hard to be clarified, after BMP4 treatment, a placenta-like state arise, the percentage of endothelial cells and primitive endoderm cell like cells increase and pluripotent cells decrease sharply. Our results not only show the ability of JGES and BMP4 in different cell lineage induction but also provide a model to explore mechanisms of first and second cell lineage decision during early embryogenesis.

2024-06-06 | GSE242851 | GEO

Cohesin chromatin loop formation by an extrinsic motor

Project description:This SuperSeries is composed of the SubSeries listed below GSE248280 contains ChIP-Seq input (IN) and IP (IP) data. GSE248281 contains micro-C in the mcool format. N1 and N2 represent repeats 1 and 2. For ChIP, Merged represent the Merged IP Merged mcool files are in supplementary files of the serie GSE248280

2024-08-04 | GSE248282 | GEO

This project is to submit 3 groups of IP-MS data for the interaction and modification differences between SALL4-pT903 and SALL4-T903 mutation during JGES somatic cell reprogramming at different time points

Project description:The 3 group of IP-MS data: D3 SALL4 IP-MS (Thermo ScientificTM Q Exactive HF-X); D1 SALL4 IP-MS between SALL4-WT and SALL4-T903A (thermo orbitrap lumos); D3 SALL4 IP-MS between NC, BMP4 treatment and Dusp9 overexpression (Q exactive HF-X).

2026-01-12 | PXD072936 |

Identification of gene targets of the transcription factor SALL4 in undifferentiated spermatogonia

Project description:Sustained spermatogenesis in adult males and recovery of fertility following germ cell depletion are dependent on undifferentiated spermatogonia with self-renewal potential. We have previously demonstrated a critical role for the transcription factor Spalt-like 4 (SALL4) in spermatogonial differentiation. However, it remains unclear whether SALL4 has broader roles within the spermatogonial pool despite its ability to co-regulate genes with PLZF, a transcription factor required for undifferentiated cell maintenance. To identify genes regulated by SALL4 in the male germline, we established cultures of undifferentiated spermatogonia from a Sall4 inducible knockout mouse model. Cells were treated with vehicle (as control) or tamoxifen to induce gene deletion, then cells harvested and analysed by microarray to identify genes mis-expressed upon loss of SALL4.

2017-08-31 | GSE98991 | GEO

dBRWD3 manipulates chromatin signature by ubiquitination to regulate ORC

Project description:Ubiquitination and epigenetic modification both play essential roles in regulating cell fates and development, but little is known how two pathways crosstalk. A known chromatin-binding protein BRWD3, Bromodomain repeats and WD40 repeats domain contain protein 3, has been shown involved both in ubiquitination and histone modification regulation. BRWD3 has roles in multiple chromatin-related processes, including transcription, DNA replication, and chromatin modification. However, how ubiquitination is involved and what’s BRWD3’s ubiquitination targets are barely known. Here, we study the single Drosophila homolog dBRWD3 to uncover its mechanism. To find dBRWD3’s ubiquitination targets, we performed both dBRWD3 IP-MS and BRWD3 dependent ubiquitination IP-MS. Expectedly, the whole BRWD3-Cul4-DDB1 E3 ubiquitination complex and multiple histones are significantly enriched in dBRWD3-IP. Interestingly, multiple histone modification writers and the DNA replication initiation factor origin recognition complex (ORC) are among the intersection of two MS. ORC’s function is highly dependent on chromatin signature. dBRWD3 could provide a perspective on how chromatin signature is regulated by ubiquitination to regulate ORC function. In support of this, about 35% of ORC2 binding sites overlap with dBRWD3 binding sites among the genome. The H3K27ac occupancy rate of dBRWD3 related ORC sites is about 50% higher than that of dBRWD3 irrelevant ORC sites. Depletion of dBRWD3 significantly reduces DNA proliferation in the S phase. Further study will focus on determining which histone modification writer is targeted for ubiquitination and how does it contribute to the chromatin signature and ORC function.

2023-10-24 | PXD039708 | Pride

Php|NF-Y transcription factor infiltrates repressive heterochromatin to generate transcripts crucial for spliceosome-dependent small RNA production

Project description:The assembly of repressive heterochromatin in eukaryotic genomes is crucial for silencing lineage-inappropriate genes and repetitive DNA elements. Paradoxically, transcription of repetitive elements within constitutive heterochromatin domains is required for RNA- based mechanisms, such as the RNAi pathway, to target heterochromatin assembly proteins. However, the mechanism by which heterochromatic repeats are transcribed has been unclear. Using fission yeast, we show that the conserved trimeric transcription factor (TF) Php|NF-Y complex, which includes histone fold domain proteins, can infiltrate constitutive heterochromatin to transcribe repeat elements. Php|NF-Y collaborates with a Zn-finger containing TF to bind repeat promoter regions with CCAAT boxes. Mutating either the TFs or the CCAAT binding site disrupts the transcription of heterochromatic repeats. Although repeat elements are transcribed from both strands, Php|NF-Y-dependent transcripts originate from only one strand. These TF-driven transcripts contain cryptic introns that are processed via a mechanism requiring the spliceosome to generate small interfering RNAs (siRNAs) by the RNAi machinery. Our analyses show that siRNA production by this TF-mediated transcription pathway is critical for heterochromatin nucleation at target repeat loci. This study reveals a mechanism by which heterochromatic repeats are transcribed, initiating their own silencing by triggering a primary cascade that produces siRNAs necessary for heterochromatin nucleation.

2024-12-06 | GSE269096 | GEO

Thalidomide promotes degradation of SALL4, a transcription factor implicated in Duane Radial Ray Syndrome, part 2

Project description:Frequently used to treat morning sickness, the drug thalidomide led to the birth of thousands of children with severe birth defects. Despite their teratogenicity, thalidomide and related IMiD drugs are now a mainstay of cancer treatment, however, the molecular basis underlying the pleiotropic biology and characteristic birth defects remains unknown. Here we show that IMiDs disrupt a broad transcriptional network through induced degradation of several C2H2 zinc finger transcription factors, including SALL4, a member of the Spalt-like family of developmental transcription factors. Strikingly, heterozygous loss of function mutations in SALL4 result in a human developmental condition that phenocopies thalidomide induced birth defects such as absence of thumbs, phocomelia, defects in ear and eye development, and congenital heart disease. We find that thalidomide induces degradation of SALL4 exclusively in humans, primates and rabbits, but not in rodents or fish, providing a mechanistic link for the species-specific pathogenesis of thalidomide syndrome.

2018-08-09 | PXD010417 | Pride

Thalidomide promotes degradation of SALL4, a transcription factor implicated in Duane Radial Ray Syndrome, part 1

2018-08-09 | PXD010416 | Pride

Thalidomide promotes degradation of SALL4, a transcription factor implicated in Duane Radial Ray Syndrome, part 6

2018-08-10 | PXD010428 | Pride

Thalidomide promotes degradation of SALL4, a transcription factor implicated in Duane Radial Ray Syndrome, part 3

2018-08-09 | PXD010418 | Pride