NRC-interacting factor directs neurite outgrowth in an activity-dependent manner. (19th March 2015)

• Record Type: Journal Article
• Authors: Zhao, X.-S.; Fu, W.-Y.; Hung, K.-W.; Chien, W.W.Y.; Li, Z.; Fu, A.K.; Ip, N.Y.
• Is Part Of: Neuroscience. Volume 289(2015)
• Page Start: 207
• Page End: 213
• Publication Date: 2015-03-19
• Subjects: AP-1 activated protein-1 -- CaMK calcium/calmodulin-dependent protein kinase -- C/EBPβ CCAAT/enhancer binding protein beta -- DIV days in vitro -- E embryonic day -- EDTA ethylenediaminetetraacetic acid -- egr-1 early growth response factor-1 -- HEPES 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid -- NIF-1 NRC-interacting factor 1 -- NRC nuclear hormone receptor coregulator -- P postnatal day -- RA retinoic acid -- RAR retinoic acid receptor -- RXR retinoid X receptor -- siRNA small interfering RNA; neuronal development -- nuclear hormone receptor -- gene transcription -- neuronal morphogenesis; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2014.12.041
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: NIF-1 is prominently expressed in the nuclei of developing neurons. NIF-1 regulates neuronal morphogenesis. NIF-1 directs gene transcription in neuronal morphogenesis in an activity-dependent manner. Abstract: Nuclear hormone receptor coregulator-interacting factor 1 (NIF-1) is a zinc finger nuclear protein that was initially identified to enhance nuclear hormone receptor transcription via its interaction with nuclear hormone receptor coregulator (NRC). NIF-1 may regulate gene transcription either by modulating general transcriptional machinery or remodeling chromatin structure through interactions with specific protein partners. We previously reported that the cytoplasmic/nuclear localization of NIF-1 is regulated by the neuronal Cdk5 activator p35, suggesting potential neuronal functions for NIF-1. The present study reveals that NIF-1 plays critical roles in regulating neuronal morphogenesis at early stages. NIF-1 was prominently expressed in the nuclei of developing rat cortical neurons. Knockdown of NIF-1 expression attenuated both neurite outgrowth in cultured cortical neurons and retinoic acid (RA)-treated Neuro-2a neuroblastoma cells. Furthermore, activity-induced Ca 2+ influx, which is critical for neuronal morphogenesis, stimulated the nuclear localization of NIF-1 in cortical neurons. Suppression of NIF-1 expression reduced the up-regulation of neuronal activity-dependent gene transcription. These findings collectively suggest that NIF-1 directs neuronal morphogenesis during early developmental stages through modulating activity-dependent gene transcription.