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The X-Linked Intellectual Disability Gene Zdhhc9 Is Essential for Dendrite Outgrowth and Inhibitory Synapse Formation.

Abstract：

:Palmitoylation is a reversible post-translational lipid modification that facilitates vesicular transport and subcellular localization of modified proteins. This process is catalyzed by ZDHHC enzymes that are implicated in several neurological and neurodevelopmental disorders. Loss-of-function mutations in ZDHHC9 have been identified in patients with X-linked intellectual disability (XLID) and associated with increased epilepsy risk. Loss of Zdhhc9 function in hippocampal cultures leads to shorter dendritic arbors and fewer inhibitory synapses, altering the ratio of excitatory-to-inhibitory inputs formed onto Zdhhc9-deficient cells. While Zdhhc9 promotes dendrite outgrowth through the palmitoylation of the GTPase Ras, it promotes inhibitory synapse formation through the palmitoylation of another GTPase, TC10. Zdhhc9 knockout mice exhibit seizure-like activity together with increased frequency and amplitude of both spontaneous and miniature excitatory and inhibitory postsynaptic currents. These findings present a plausible mechanism for how the loss of ZDHHC9 function may contribute to XLID and epilepsy.

journal_name

Cell Rep

journal_title

Cell reports

authors

Shimell JJ,Shah BS,Cain SM,Thouta S,Kuhlmann N,Tatarnikov I,Jovellar DB,Brigidi GS,Kass J,Milnerwood AJ,Snutch TP,Bamji SX

doi

10.1016/j.celrep.2019.10.065

subject

Has Abstract

pub_date

2019-11-19 00:00:00

pages

2422-2437.e8

issue

8

issn

2211-1247

pii

S2211-1247(19)31379-8

journal_volume

29

pub_type

杂志文章

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