English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
  TIP60/KAT5 is required for neuronal viability in hippocampal CA1.

Urban, I., Kerimoglu, C., Sakib, M. S., Wang, H., Benito, E., Thaller, C., et al. (2019). TIP60/KAT5 is required for neuronal viability in hippocampal CA1. Scientific Reports, 9: 16173. doi:10.1038/s41598-019-50927-1.

Item is

Files

show Files
hide Files
:
3175912.pdf (Publisher version), 5MB
Name:
3175912.pdf
Description:
-
OA-Status:
Visibility:
Public
MIME-Type / Checksum:
application/pdf / [MD5]
Technical Metadata:
Copyright Date:
-
Copyright Info:
-
:
3175912_Suppl.htm (Supplementary material), 376KB
Name:
3175912_Suppl.htm
Description:
-
OA-Status:
Visibility:
Public
MIME-Type / Checksum:
text/html / [MD5]
Technical Metadata:
Copyright Date:
-
Copyright Info:
-
License:
-

Locators

show

Creators

show
hide
 Creators:
Urban, I.1, Author           
Kerimoglu, C., Author
Sakib, M. S., Author
Wang, H., Author
Benito, E., Author
Thaller, C.1, Author           
Zhou, X., Author
Yan, J., Author
Fischer, A., Author
Eichele, G.1, Author           
Affiliations:
1Department of Genes and Behavior, MPI for Biophysical Chemistry, Max Planck Society, ou_persistent34              

Content

show
hide
Free keywords: -
 Abstract: Aberrant histone acetylation contributes to age-dependent cognitive decline and neurodegenerative diseases. We analyze the function of lysine acetyltransferase TIP60/KAT5 in neurons of the hippocampus using an inducible mouse model. TIP60-deficiency in the adult forebrain leads within days to extensive transcriptional dysfunction characterized by the presence of a neurodegeneration-related signature in CA1. Cell cycle- and immunity-related genes are upregulated while learning- and neuronal plasticity-related genes are downregulated. The dysregulated genes seen under TIP60-deficiency overlap with those in the well-characterized CK-p25 neurodegeneration model. We found that H4K12 is hypoacetylated at the transcriptional start sites of those genes whose expression is dampened in TIP60-deficient mice. Transcriptional dysregulation is followed over a period of weeks by activation of Caspase 3 and fragmentation of β-actin in CA1 neurites, eventually leading to severe neuronal loss. TIP60-deficient mice also develop mild memory impairment. These phenotypes point to a central role of TIP60 in transcriptional networks that are critical for neuronal viability.

Details

show
hide
Language(s): eng - English
 Dates: 2019-11-07
 Publication Status: Published online
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1038/s41598-019-50927-1
 Degree: -

Event

show

Legal Case

show

Project information

show

Source 1

show
hide
Title: Scientific Reports
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: -
Pages: 15 Volume / Issue: 9 Sequence Number: 16173 Start / End Page: - Identifier: -