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2 results on '"H4K20 acetylation"'

1. The histone deacetylase complex MiDAC regulates a neurodevelopmental gene expression program to control neurite outgrowth

Author

Hans-Martin Herz, Hongjian Jin, Tanner Martinez, Yurii Sedkov, Greg J Poet, Shondra M. Pruett-Miller, Chunliang Li, Satish Kallappagoudar, Monica F. Sentmanat, Yiping Fan, and Baisakhi Mondal

Subjects
0301 basic medicine, Male, Neurite, Mouse, QH301-705.5, Science, Neuronal Outgrowth, Biology, ELMSAN1/MIDEAS, General Biochemistry, Genetics and Molecular Biology, Histone Deacetylases, 03 medical and health sciences, Mice, 0302 clinical medicine, H4K20 acetylation, neurite ourgrowth, Gene expression, Animals, Biology (General), Enhancer, Mice, Knockout, General Immunology and Microbiology, General Neuroscience, Neurogenesis, Membrane Proteins, Cell Differentiation, General Medicine, DNA Methylation, Netrin-1, Chromosomes and Gene Expression, DNTTIP1, HDAC1, Cell biology, Mice, Inbred C57BL, 030104 developmental biology, Midac, Gene Expression Regulation, Histone deacetylase complex, H3K27 acetylation, Medicine, Histone deacetylase, 030217 neurology & neurosurgery, Research Article, Neuroscience, mitotic deacetylase complex MiDAC, SLIT and NETRIN signaling pathways
Abstract

The mitotic deacetylase complex (MiDAC) is a recently identified histone deacetylase (HDAC) complex. While other HDAC complexes have been implicated in neurogenesis, the physiological role of MiDAC remains unknown. Here, we show that MiDAC constitutes an important regulator of neural differentiation. We demonstrate that MiDAC functions as a modulator of a neurodevelopmental gene expression program and binds to important regulators of neurite outgrowth. MiDAC upregulates gene expression of pro-neural genes such as those encoding the secreted ligands SLIT3 and NETRIN1 (NTN1) by a mechanism suggestive of H4K20ac removal on promoters and enhancers. Conversely, MiDAC inhibits gene expression by reducing H3K27ac on promoter-proximal and -distal elements of negative regulators of neurogenesis. Furthermore, loss of MiDAC results in neurite outgrowth defects that can be rescued by supplementation with SLIT3 and/or NTN1. These findings indicate a crucial role for MiDAC in regulating the ligands of the SLIT3 and NTN1 signaling axes to ensure the proper integrity of neurite development.

Published
2020

2. The histone deacetylase complex MiDAC regulates a neurodevelopmental gene expression program to control neurite outgrowth.

Author

Mondal B, Jin H, Kallappagoudar S, Sedkov Y, Martinez T, Sentmanat MF, Poet GJ, Li C, Fan Y, Pruett-Miller SM, and Herz HM

Subjects
Animals, Cell Differentiation physiology, DNA Methylation physiology, Male, Membrane Proteins metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Netrin-1 metabolism, Gene Expression Regulation physiology, Histone Deacetylases metabolism, Neuronal Outgrowth physiology
Abstract

The mitotic deacetylase complex (MiDAC) is a recently identified histone deacetylase (HDAC) complex. While other HDAC complexes have been implicated in neurogenesis, the physiological role of MiDAC remains unknown. Here, we show that MiDAC constitutes an important regulator of neural differentiation. We demonstrate that MiDAC functions as a modulator of a neurodevelopmental gene expression program and binds to important regulators of neurite outgrowth. MiDAC upregulates gene expression of pro-neural genes such as those encoding the secreted ligands SLIT3 and NETRIN1 (NTN1) by a mechanism suggestive of H4K20ac removal on promoters and enhancers. Conversely, MiDAC inhibits gene expression by reducing H3K27ac on promoter-proximal and -distal elements of negative regulators of neurogenesis. Furthermore, loss of MiDAC results in neurite outgrowth defects that can be rescued by supplementation with SLIT3 and/or NTN1. These findings indicate a crucial role for MiDAC in regulating the ligands of the SLIT3 and NTN1 signaling axes to ensure the proper integrity of neurite development., Competing Interests: BM, HJ, SK, YS, TM, MS, GP, CL, YF, SP, HH No competing interests declared, (© 2020, Mondal et al.)

Published
2020
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