Current research by Herr et al (2006) has shown RNA silencing pathways may be induced via defective RNA transcription, consequently affecting the flowering time in Arabidopsis.
The study was conducted using enhanced silencing phenotype (esp) mutant Arabidopsis plants and it has been identified that proteins involved in RNA transcript processing and 3’ end formation can activate RNA silencing pathways. Two such proteins, symplekin/PTA1 homologue and CPSF100 in Arabidopsis form part a complex with FY, a protein important in the regulation of FCA processing. Where FY is defective, misprocessing of FCA can occur. Consequently, the autoregulated alternate splicing mechanism in 3’ end formation is affected and increased silencing of the FCA-β mRNA transcript occurs. Interestingly, early flowering in the esp mutant is also observed.
In the esp mutants, FCA-β mRNA is silenced in a RDR6-dependent manner and thus Herr et al (2006) reached the conclusion that small interfering (siRNA) are produced from aberrant FCA-β RNA and is the causative agent initiating RNA silencing. It was also suggested that the siRNAs produced from aberrant FCA-β RNA may also silence the flowering suppressor genes, which provides an explanation for the early flowering observed in mutant phenotypes.
The overall findings of research have correlated increased RNA silencing as a result of defective transcript processing, which subsequently influences flowering time control in Arabidopsis.
Sarah Woolner, 41014420
Reference:
Herr AJ, Molnàr A, Jones A, Baulcombe DC (2006). Defective RNA processing enhances RNA silencing and influences flowering of Arabidopsis. Proc Natl Acad Sci U S A. 103(41):14994-5001.
