AUTHOR=Li Linxuan , Song Yun , Wang Kai , Dong Pan , Zhang Xueyan , Li Fuguang , Li Zhengguo , Ren Maozhi 

TITLE=TOR-inhibitor insensitive-1 (TRIN1) regulates cotyledons greening in Arabidopsis

JOURNAL=Frontiers in Plant Science

VOLUME=6

YEAR=2015

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2015.00861

DOI=10.3389/fpls.2015.00861

ISSN=1664-462X

ABSTRACT=<p>Target of Rapamycin (TOR) is an eukaryotic protein kinase and evolutionally conserved from the last eukaryotic common ancestor (LECA) to humans. The growing evidences have shown that TOR signaling acts as a central controller of cell growth and development. The downstream effectors of TOR have been well-identified in yeast and animals by using the immunosuppression agent rapamycin. However, less is known about TOR in plants. This is largely due to the fact that plants are insensitive to rapamycin. In this study, AZD8055 (AZD), the novel ATP-competitive inhibitor of TOR, was employed to decipher the downstream effectors of TOR in <italic>Arabidopsis</italic>. One AZD insensitive mutant, <bold><italic>T</italic></bold><italic>O</italic><bold><italic>R</italic></bold><italic>-</italic><bold><italic>i</italic></bold><italic>nhibitor i</italic><bold><italic>n</italic></bold><italic>sensitive-</italic><bold><italic>1</italic></bold> (<italic>trin1</italic>), was screened from 10,000 EMS-induced mutation seeds. The cotyledons of <italic>trin1</italic> can turn green when its seeds were germinated on ½ MS medium supplemented with 2 μM AZD, whereas the cotyledons greening of wild-type (WT) can be completely blocked at this concentration. Through genetic mapping, <italic>TRIN1</italic> was mapped onto the long arm of chromosome 2, between markers SGCSNP26 and MI277. Positional cloning revealed that <italic>TRIN1</italic> was an allele of <italic>ABI4</italic>, which encoded an ABA-regulated AP2 domain transcription factor. Plants containing <italic>P35S::TRIN1</italic> or <italic>P35S::TRIN1-GUS</italic> were hypersensitive to AZD treatment and displayed the opposite phenotype observed in <italic>trin1</italic>. Importantly, GUS signaling was significantly enhanced in <italic>P35S::TRIN1-GUS</italic> transgenic plants in response to AZD treatment, indicating that suppression of TOR resulted in the accumulation of TRIN1. These observations revealed that TOR controlled seed-to-seedling transition by negatively regulating the stability of TRIN1 in <italic>Arabidopsis</italic>. For the first time, TRIN1, the downstream effector of TOR signaling, was identified through a chemical genetics approach.</p>