Format

Send to

Choose Destination
Dev Cell. 2016 Jul 25;38(2):186-200. doi: 10.1016/j.devcel.2016.06.008. Epub 2016 Jul 7.

N(6)-Methyladenosine RNA Modification Regulates Shoot Stem Cell Fate in Arabidopsis.

Author information

1
Temasek Life Sciences Laboratory and Department of Biological Sciences, National University of Singapore, 10 Science Drive 4, Singapore 117543, Singapore.
2
Biotechnology Research Institute, Chinese Academy of Agricultural Sciences, Beijing 100081, China.
3
South China Botanical Garden, Chinese Academy of Sciences, Guangzhou 510650, China.
4
Singapore-MIT Alliance for Research and Technology, Campus for Research Excellence and Technical Enterprise (CREATE), Singapore 138602, Singapore.
5
Temasek Life Sciences Laboratory and Department of Biological Sciences, National University of Singapore, 10 Science Drive 4, Singapore 117543, Singapore. Electronic address: dbsyuhao@nus.edu.sg.

Abstract

N(6)-Methyladenosine (m(6)A) represents the most prevalent internal modification on mRNA and requires a multicomponent m(6)A methyltransferase complex in mammals. How their plant counterparts determine the global m(6)A modification landscape and its molecular link to plant development remain unknown. Here we show that FKBP12 INTERACTING PROTEIN 37 KD (FIP37) is a core component of the m(6)A methyltransferase complex, which underlies control of shoot stem cell fate in Arabidopsis. The mutants lacking FIP37 exhibit massive overproliferation of shoot meristems and a transcriptome-wide loss of m(6)A RNA modifications. We further demonstrate that FIP37 mediates m(6)A RNA modification on key shoot meristem genes inversely correlated with their mRNA stability, thus confining their transcript levels to prevent shoot meristem overproliferation. Our results suggest an indispensable role of FIP37 in mediating m(6)A mRNA modification, which is required for maintaining the shoot meristem as a renewable source for continuously producing all aerial organs in plants.

PMID:
27396363
PMCID:
PMC6364302
DOI:
10.1016/j.devcel.2016.06.008
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center