Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1)
The RNA-binding protein Snd1/Tudor-SN regulates hypoxia-responsive gene expression
Julkaisun tekijät: Saarikettu Juha, Lehmusvaara Saara, Pesu Marko, Junttila Ilkka, Partanen Juha, Sipilä Petra, Poutanen Matti, Yang Jie, Haikarainen Teemu, Silvennoinen Olli
Kustantaja: Wiley
Julkaisuvuosi: 2023
Journal: FASEB BioAdvances
Tietokannassa oleva lehden nimi: FASEB BIOADVANCES
Lehden akronyymi: FASEB BIOADV
Sivujen määrä: 16
eISSN: 2573-9832
DOI: http://dx.doi.org/10.1096/fba.2022-00115
Verkko-osoite: https://faseb.onlinelibrary.wiley.com/doi/10.1096/fba.2022-00115
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/179066916
Snd1 is an evolutionarily conserved RNA-binding protein implicated in several regulatory processes in gene expression including activation of transcription, mRNA splicing, and microRNA decay. Here, we have investigated the outcome of Snd1 gene deletion in the mouse. The knockout mice are viable showing no gross abnormalities apart from decreased fertility, organ and body size, and decreased number of myeloid cells concomitant with decreased expression of granule protein genes. Deletion of Snd1 affected the expression of relatively small number of genes in spleen and liver. However, mRNA expression changes in the knockout mouse liver showed high similarity to expression profile in adaptation to hypoxia. MicroRNA expression in liver showed upregulation of the hypoxia-induced microRNAs miR-96 and -182. Similar to Snd1 deletion, mimics of miR-96/182 enhanced hypoxia-responsive reporter activity. To further elucidate the function of SND1, BioID biotin proximity ligation assay was performed in HEK-293T cells to identify interacting proteins. Over 50% of the identified interactors were RNA-binding proteins, including stress granule proteins. Taken together, our results show that in normal growth conditions, Snd1 is not a critical factor for mRNA transcription in the mouse, and describe a function for Snd1 in hypoxia adaptation through negatively regulating hypoxia-related miRNAs and hypoxia-induced transcription consistent with a role as stress response regulator.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
