Project description:Sall4 is among one of the most important reprogramming factors. However, the underline molecular mechanisms for such importance remains unclear. In this report, we first described the gene expression and chromatin accessibility dynamics in OKS-Sall4 induced somatic cell reprogramming, and screened a group of downstream targets of Sall4, among which, cecr2, regulated by Sall4 directly, can significantly promote OKS induced reprogramming. Moreover, Cecr2 and Sall4 shared several downstream targets, such as Esrrb, Nanog, T etc., at transcription level when overexpress in the context of OKS induced reprogramming. We further showed that the DTT domain of cecr2 was responding to the reprogramming activity. Our findings provide a new important reprogramming factors and suggesting the cecr2-associted protein network may contributes to overcoming the epigenetic barriers in reprogramming.
Project description:Sall4 is among one of the most important reprogramming factors. However, the underline molecular mechanisms for such importance remains unclear. In this report, we first described the gene expression and chromatin accessibility dynamics in OKS-Sall4 induced somatic cell reprogramming, and screened a group of downstream targets of Sall4, among which, cecr2, regulated by Sall4 directly, can significantly promote OKS induced reprogramming. Moreover, Cecr2 and Sall4 shared several downstream targets, such as Esrrb, Nanog, T etc., at transcription level when overexpress in the context of OKS induced reprogramming. We further showed that the DTT domain of cecr2 was responding to the reprogramming activity. Our findings provide a new important reprogramming factors and suggesting the cecr2-associted protein network may contributes to overcoming the epigenetic barriers in reprogramming.
Project description:Sall4 is among one of the most important reprogramming factors. However, the underline molecular mechanisms for such importance remains unclear. In this report, we first described the gene expression and chromatin accessibility dynamics in OKS-Sall4 induced somatic cell reprogramming, and screened a group of downstream targets of Sall4, among which, cecr2, regulated by Sall4 directly, can significantly promote OKS induced reprogramming. Moreover, Cecr2 and Sall4 shared several downstream targets, such as Esrrb, Nanog, T etc., at transcription level when overexpress in the context of OKS induced reprogramming. We further showed that the DTT domain of cecr2 was responding to the reprogramming activity. Our findings provide a new important reprogramming factors and suggesting the cecr2-associted protein network may contributes to overcoming the epigenetic barriers in reprogramming.
Project description:Purpose: Metastasis are responsible for the most majority of cancer-related deaths due to the lack of effective targeted therapies. Therefore, specific targets which tackle that complex process are needed to improve the therapeutic outcomes of metastatic breast cancer. Methods: ATAC-Seq analysis of CECR2 knockout and control LM2 cells. Results: CECR2 knockout regulate chromatin accessibility of NF-kB target genes . Conclusions: Our work confirmed that CECR2 knockout attenuates chromatin accessibility at promoters or enhancers of the downstream NF-kB target genes.
Project description:Cell fate decision involves rewiring of the genome, but remains poorly understood at the chromatin level. We report a system to reprogramming somatic cells to pluripotency by four factor combination (Sall4, Esrrb, Jdp2, Glis1). Mechanism study demonstrate that the Sall4-NuRD axis plays a critical role in the early phase of reprogramming. These results identify a previously unrecognized role of NuRD in reprogramming, may help establish early chromatin closing as a pre-requisite step in cell fate control.
Project description:Cell fate decision involves rewiring of the genome, but remains poorly understood at the chromatin level. We report a system to reprogramming somatic cells to pluripotency by four factor combination (Sall4, Esrrb, Jdp2, Glis1). Mechanism study demonstrate that the Sall4-NuRD axis plays a critical role in the early phase of reprogramming. These results identify a previously unrecognized role of NuRD in reprogramming, may help establish early chromatin closing as a pre-requisite step in cell fate control.