The Eating-Disorder Associated HDAC4^A778T Mutation Alters Feeding Behaviors in Female Mice.

ABSTRACT:

Background

While eating disorders (EDs) are thought to result from a combination of environmental and psychological stressors superimposed on genetic vulnerability, the neurobiological basis of EDs remains incompletely understood. We recently reported that a rare missense mutation in the gene for the transcriptional repressor histone deacetylase 4 (HDAC4) is associated with the risk of developing an ED in humans.

Methods

To understand the biological consequences of this missense mutation, we created transgenic mice carrying this mutation by introducing the alanine to threonine mutation at position 778 of mouse Hdac4 (corresponding to position 786 of the human protein). Bioinformatic analysis to identify Hdac4-regulated genes was performed using available databases.

Result

SUBMITTER: Lutter M 

PROVIDER: S-EPMC5386818 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature