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The RNA Binding Protein ELF9 Directly Reduces SUPPRESSOR OF OVEREXPRESSION OF CO1 Transcript
 

Summary: The RNA Binding Protein ELF9 Directly Reduces
SUPPRESSOR OF OVEREXPRESSION OF CO1 Transcript
Levels in Arabidopsis, Possibly via Nonsense-Mediated
mRNA Decay W
Hae-Ryong Song,a,b Ju-Dong Song,a Jung-Nam Cho,a,b Richard M. Amasino,b,c Bosl Noh,b,d,1 and Yoo-Sun Noha,b,1
a School of Biological Sciences, Seoul National University, Seoul 151-747, Korea
b Global Research Laboratory for Floral Regulatory Signaling, Seoul National University, Seoul 151-747, Korea
c Department of Biochemistry, University of Wisconsin, Madison, Wisconsin 53706
d Environmental Biotechnology National Core Research Center, Gyeongsang National University, Jinju 660-701, Korea
SUPPRESSOR OF OVEREXPRESSION OF CO1 (SOC1) is regulated by a complex transcriptional regulatory network that
allows for the integration of multiple floral regulatory inputs from photoperiods, gibberellin, and FLOWERING LOCUS C.
However, the posttranscriptional regulation of SOC1 has not been explored. Here, we report that EARLY FLOWERING9
(ELF9), an Arabidopsis thaliana RNA binding protein, directly targets the SOC1 transcript and reduces SOC1 mRNA levels,
possibly through a nonsense-mediated mRNA decay (NMD) mechanism, which leads to the degradation of abnormal
transcripts with premature translation termination codons (PTCs). The fully spliced SOC1 transcript is upregulated in elf9
mutants as well as in mutants of NMD core components. Furthermore, a partially spliced SOC1 transcript containing a PTC
is upregulated more significantly than the fully spliced transcript in elf9 in an ecotype-dependent manner. A Myc-tagged
ELF9 protein (MycELF9) directly binds to the partially spliced SOC1 transcript. Previously known NMD target transcripts of
Arabidopsis are also upregulated in elf9 and recognized directly by MycELF9. SOC1 transcript levels are also increased by
the inhibition of translational activity of the ribosome. Thus, the SOC1 transcript is one of the direct targets of ELF9, which

  

Source: Amasino, Richard M. - Department of Biochemistry, University of Wisconsin at Madison

 

Collections: Biology and Medicine