@article{oai:shiga-med.repo.nii.ac.jp:00003515,
 author = {門田, 陽介 and 雪上, 晴加 and 寺門, 一郎 and 森宗, 孝夫 and 田埜, 郁実 and 田中, 雄也 and 赤羽, 紗由美 and 福村, 真優 and 遠山, 育夫 and 森, 雅樹 and KADOTA, Yosuke and JAM, Faidruz Azura and YUKIUE, Haruka and TERAKADO, Ichiro and MORIMUNE, Takao and TANO, Ayami and TANAKA, Yuya and AKAHANE, Sayumi and FUKUMURA, Mayu and TOOYAMA, Ikuo and MORI, Masaki},
 issue = {3},
 journal = {iScience},
 month = {Mar},
 note = {The juvenile phase is characterized by continuously progressing physiological processes such as growth and maturation, which are accompanied by transitions in gene expression. The contribution of transcriptome dynamics to the establishment of juvenile properties remains unclear. Here, we investigated alternative splicing (AS) events in postnatal growth and elucidated the landscape of age-dependent alternative splicing (ADAS) in C57BL/6 mice. Our analysis of ADAS in the cerebral cortex, cardiomyocytes, and hepatocytes revealed numerous juvenile-specific splicing isoforms that shape the juvenile transcriptome, which in turn functions as a basis for the highly anabolic status of juvenile cells. Mechanistically, the juvenile-expressed splicing factor Srsf7 mediates ADAS, as exemplified by switching from juvenile to adult forms of anabolism-associated genes Eif4a2 and Rbm7. Suppression of Srsf7 results in "fast-forwarding" of this transcriptome transition, causing impaired anabolism and growth in mice. Thus, juvenile-specific AS is indispensable for the anabolic state of juveniles and differentiates juveniles from adults., Journal Article},
 title = {Srsf7 Establishes the Juvenile Transcriptome through Age-Dependent Alternative Splicing in Mice.},
 volume = {23},
 year = {2020}
}