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14-3-3 α and 14-3-3 ζ contribute to immune responses in planarian Dugesia japonica

14-3-3 proteins are a family of highly conserved acidic proteins that regulate cellular processes. They act as a kind of important signaling molecules taking part in many crucial decisions throughout the development process. We have isolated and characterized two members of the 14-3-3 family, namely...

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Published in:Gene 2017-06, Vol.615, p.25-34
Main Authors: Lu, Qingqing, Wu, Suge, Zhen, Hui, Deng, Hongkuan, Song, Qian, Ma, Kaifu, Cao, Zhonghong, Pang, Qiuxiang, Zhao, Bosheng
Format: Article
Language:English
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Summary:14-3-3 proteins are a family of highly conserved acidic proteins that regulate cellular processes. They act as a kind of important signaling molecules taking part in many crucial decisions throughout the development process. We have isolated and characterized two members of the 14-3-3 family, namely, Dj14-3-3 α and Dj14-3-3 ζ in the planarian Dugesia japonica. The Dj14-3-3 α and ζ genes encode polypeptides of 260 and 255 amino acids respectively. We have proved that the Dj14-3-3 α and ζ genes were especially expressed in the pharynx in adult and regenerating planarians by in situ hybridization and they were not involved in regeneration process. Besides, Dj14-3-3 α and ζ genes can compensate each other in planarians by RNA interference. The Dj14-3-3 α and ζ were significantly up-regulated expression when planarians were stimulated with the pathogen-associated molecular patterns including lipopolysaccharide (LPS), peptidoglycan (PGN), β-Glu and Poly (I:C), indicating that the Dj14-3-3 α and ζ may be involved in the immune responses. •Both 14-3-3 α and 14-3-3 ζ (Dj14-3-3 α and Dj14-3-3 ζ) genes were isolated and characterized from planarian Dugesia japonica.•Dj14-3-3 α and Dj14-3-3 ζ are predominantly expressed in the pharynx of intact and regenerating planarians.•Loss function of Dj14-3-3 α and ζ by RNA interference during planarian regeneration did not affect the pharynx regeneration.•Dj14-3-3 α and ζ may participate in the immune response upon pathogen invasion.
ISSN:0378-1119
1879-0038
DOI:10.1016/j.gene.2017.03.017