Asset Details
Do you wish to reserve the book?
KAT6B overexpression rescues embryonic lethality in homozygous null KAT6A mice restoring vitality and normal lifespan
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
KAT6B overexpression rescues embryonic lethality in homozygous null KAT6A mice restoring vitality and normal lifespan
Do you wish to request the book?
KAT6B overexpression rescues embryonic lethality in homozygous null KAT6A mice restoring vitality and normal lifespan
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
KAT6B overexpression rescues embryonic lethality in homozygous null KAT6A mice restoring vitality and normal lifespan
2025
Overview
Closely related genes typically display common essential functions but also functional diversification, ensuring retention of both genes throughout evolution. The histone lysine acetyltransferases KAT6A (MOZ) and KAT6B (QKF/MORF), sharing identical protein domain structure, are mutually exclusive catalytic subunits of a multiprotein complex. Mutations in either
KAT6A
or
KAT6B
result in congenital intellectual disability disorders in human patients. In mice, loss of function of either gene results in distinct, severe phenotypic consequences. Here we show that, surprisingly, 4-fold overexpression of
Kat6b
rescues all previously described developmental defects in
Kat6a
mutant mice, including rescuing the absence of hematopoietic stem cells.
Kat6b
restores acetylation at histone H3 lysines 9 and 23 and reverses critical gene expression anomalies in
Kat6a
mutant mice. Our data suggest that the target gene specificity of KAT6A can be substituted by the related paralogue KAT6B, despite differences in amino acid sequence, if KAT6B is expressed at sufficiently high levels.
KAT6A and KAT6A are epigenetic regulators with critical functions in embryonic development. Mutations in either KAT6A or KAT6B result in distinct congenital disorders in human patients. Surprisingly, overexpression of KAT6B can rescue loss of KAT6A.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/31
/ 38/15
/ 38/39
/ 64/110
/ 64/60
/ Animals
/ Female
/ Gene Expression Regulation, Developmental
/ Genes
/ Hematopoietic Stem Cells - metabolism
/ Histone Acetyltransferases - genetics
/ Histone Acetyltransferases - metabolism
/ Histones
/ Humanities and Social Sciences
/ Humans
/ Lysine
/ Lysine Acetyltransferases - genetics
/ Lysine Acetyltransferases - metabolism
/ Male
/ Mice
/ Mutants
/ Mutation
/ Science
