NDLI: Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Chen, Shaowei Yao, Xiao Li, Yuwen Saifudeen, Zubaida Bachvarov, Dimcho El-Dahr, Samir S.
Description	Country affiliation: United States Author Affiliation: Chen S ( Department of Pediatrics, Section of Pediatric Nephrology, Tulane University Health Sciences Center, New Orleans, LA 70112, USA.); Yao X ( Department of Pediatrics, Section of Pediatric Nephrology, Tulane University Health Sciences Center, New Orleans, LA 70112, USA.); Li Y ( Department of Pediatrics, Section of Pediatric Nephrology, Tulane University Health Sciences Center, New Orleans, LA 70112, USA.); Saifudeen Z ( Department of Pediatrics, Section of Pediatric Nephrology, Tulane University Health Sciences Center, New Orleans, LA 70112, USA.); Bachvarov D ( Department of Molecular Medicine, Laval University, Québec, QC, Canada G1R 2J6.); El-Dahr SS ( Department of Pediatrics, Section of Pediatric Nephrology, Tulane University Health Sciences Center, New Orleans, LA 70112, USA seldahr@tulane.edu.)
Abstract	Histone deacetylases (HDACs) regulate a broad range of biological processes through removal of acetyl groups from histones as well as non-histone proteins. Our previous studies showed that Hdac1 and Hdac2 are bound to promoters of key renal developmental regulators and that HDAC activity is required for embryonic kidney gene expression. However, the existence of many HDAC isoforms in embryonic kidneys raises questions concerning the possible specificity or redundancy of their functions. We report here that targeted deletion of both the Hdac1 and Hdac2 genes from the ureteric bud (UB) cell lineage of mice causes bilateral renal hypodysplasia. One copy of either Hdac1 or Hdac2 is sufficient to sustain normal renal development. In addition to defective cell proliferation and survival, genome-wide transcriptional profiling revealed that the canonical Wnt signaling pathway is specifically impaired in UB(Hdac1,2-/-) kidneys. Our results also demonstrate that loss of Hdac1 and Hdac2 in the UB epithelium leads to marked hyperacetylation of the tumor suppressor protein p53 on lysine 370, 379 and 383; these post-translational modifications are known to boost p53 stability and transcriptional activity. Genetic deletion of p53 partially rescues the development of UB(Hdac1,2-/-) kidneys. Together, these data indicate that Hdac1 and Hdac2 are crucial for kidney development. They perform redundant, yet essential, cell lineage-autonomous functions via p53-dependent and -independent pathways.
File Format	HTM / HTML
ISSN	09501991
e-ISSN	14779129
DOI	10.1242/dev.113506
Journal	Development
Issue Number	6
Volume Number	142
Language	English
Publisher	The Company of Biologists
Publisher Date	2015-03-15
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Developmental Discipline Biology Gene Expression Regulation, Developmental Physiology Histone Deacetylase 1 Metabolism Histone Deacetylase 2 Signal Transduction Tumor Suppressor Protein P53 Ureter Embryology Wnt Proteins Acetylation Animals Blotting, Western Flow Cytometry Gene Expression Profiling Genetics Gene Knockout Techniques Histological Techniques Immunohistochemistry In Situ Hybridization Mice Mice, Transgenic Microarray Analysis Real-time Polymerase Chain Reaction Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Developmental Biology Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium

Compensatory functions of histone deacetylase 1 (HDAC1) and HDAC2 regulate transcription and apoptosis during mouse oocyte development

Deacetylation of p53 induces autophagy by suppressing Bmf expression

Histone deacetylase (HDAC) 1 and 2 are essential for accurate cell division and the pluripotency of embryonic stem cells.

Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractility.

Histone deacetylase 2 controls p53 and is a critical factor in tumorigenesis

Histone deacetylase HDAC1/HDAC2-controlled embryonic development and cell differentiation.

Sall1-dependent signals affect Wnt signaling and ureter tip fate to initiate kidney development

Histone Cross-talk Connects Protein Phosphatase 1α (PP1α) and Histone Deacetylase (HDAC) Pathways to Regulate the Functional Transition of Bromodomain-containing 4 (BRD4) for Inducible Gene Expression

Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium.

Similar Documents

Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium

Compensatory functions of histone deacetylase 1 (HDAC1) and HDAC2 regulate transcription and apoptosis during mouse oocyte development

Deacetylation of p53 induces autophagy by suppressing Bmf expression

Histone deacetylase (HDAC) 1 and 2 are essential for accurate cell division and the pluripotency of embryonic stem cells.

Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractility.

Histone deacetylase 2 controls p53 and is a critical factor in tumorigenesis

Histone deacetylase HDAC1/HDAC2-controlled embryonic development and cell differentiation.

Sall1-dependent signals affect Wnt signaling and ureter tip fate to initiate kidney development

Histone Cross-talk Connects Protein Phosphatase 1α (PP1α) and Histone Deacetylase (HDAC) Pathways to Regulate the Functional Transition of Bromodomain-containing 4 (BRD4) for Inducible Gene Expression

Histone deacetylase 1 and 2 regulate Wnt and p53 pathways in the ureteric bud epithelium.