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Updated: Jan 28, 2026

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
Published on: April 29, 2010
Regulation of chromatin remodeling through RNA polymerase II stalling in the immune system
Zuli Wang1, Shuang Liu2, Yongguang Tao1
1Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan, 410008, China; Key Laboratory of Carcinogenesis, Ministry of Health, Cancer Research Institute, Central South University, 110 Xiangya Road, Changsha, Hunan, 410078, China; Department of Thoracic Surgery, Second Xiangya Hospital, Central South University, Changsha, China.
Abstract:
RNA polymerase II (Pol II) binds to promoter-proximal regions of inducible target genes that are controlled and not transcribed by several negative elongation factors, which is known as Pol II stalling. The occurrence of stalling is due to particular modification signatures and structural conformations of chromatin that affect Pol II elongation. The existence and physiological importance of Pol II stalling implies that there is a dynamic balance in chromatin regulation prior to endogenous or exogenous stimulation. In this review, we discuss the effects of ATP-dependent chromatin remodeling complexes and histone modification via transcriptional machinery Pol II C-terminal domain phosphorylated at serine 5 (S5P RNAPII) initiation and S2P RNAPII elongation on the expression or silence of specific genes after the production of activated or differentiated signals or cytokines. The response occurs immediately during immune cell development and function, and it also includes the generation of immunological memories. This summary suggests that the host immune response genes involve a novel mechanism of selectively regulatory chromatin remodeling, a fundamental and crucial aspect of epigenetic regulation.
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