Pou1f1, the key transcription factor related to somatic growth in tilapia (Orechromis niloticus), is regulated by two independent post-transcriptional regulation mechanisms
Pou1f1, the key transcription factor related to somatic growth in tilapia (Orechromis niloticus), is regulated by two independent post-transcriptional regulation mechanisms
复制标题
Pou1f1是与罗非鱼（Orechromis niloticus）体细胞生长相关的关键转录因子，受到两种独立的转录后调控机制的调控
DOI：
10.1016/j.bbrc.2016.12.106
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发表时间：
2017
影响因子：
3.1
通讯作者：
Li Wensheng
中科院分区：
文献类型：
--
作者：
Wang Dongfang;Qin Jingkai;Jia Jirong;Yan Peipei;Li Wensheng
This study aims to determine the post-transcriptional regulation mechanism of the transcription factorpou1f1(pou class 1homeobox1), which is the key gene for pituitary development, somatic growth in vertebrates, and transcription of several hormone genes in teleost fish. MicroRNAmiR-223-3pwas identified as abona fidetarget ofpou1f; overexpression ofmiR-223-3pin primary pituitary cells led to the down-regulation ofpou1f1and downstream genes, and inhibition ofmiR-223-3pled to the up-regulation ofpou1f1in Nile tilapia dispersed primary pituitary cells. An adenylate-uridylate-rich element (AU-Rich element) was found in the 3′UTR ofpou1f1mRNA, and deletion of the AU-Rich element led to slower mRNA decay and therefore more protein output. A potential mutual relationship betweenmiR-223-3pand the AU-rich element was also investigated, and the results demonstrated that with or without the AU-Rich element,miR-223-3pinduced the up-regulation of a reporter system under serum starvation conditions, indicating thatmiR-223-3pand the AU-Rich element function independent of each other. This study is the first to investigate the post-transcriptional mechanism ofpou1f1, which revealed thatmiR-223-3pdown-regulatedpou1f1and downstream gene expressions, and the AU-Rich element led to rapid decay ofpou1f1mRNA. MicroRNAmiR-223-3pand the AU-Rich element co-regulated the post-transcriptional expression ofpou1f1independently in Nile tilapia, demonstrating thatpou1f1is under the control of a dual post-transcription regulation mechanism.
