ABA induction of miR159 controls transcript levels of two MYB factors during Arabidopsis seed germination

TLDR

During seed imbibition ABA levels fall to permit germination, but under stress they remain high and arrest growth, a process regulated by transcription factors such as ABI3 and ABI5. The study investigates whether ABA induces miR159 in an ABI3‑dependent manner and whether miR159 mediates cleavage of MYB101 and MYB33 transcripts. The authors find that ABA‑induced miR159 promotes degradation of MYB33 and MYB101, whose loss or suppression reduces ABA sensitivity, while resistance to miR159 or viral inhibition of miRNA function increases ABA sensitivity, indicating that miR159 acts as a homeostatic regulator of ABA signaling during seedling stress.

Abstract

Summary Upon seed imbibition, abscisic acid (ABA) levels decrease to allow embryos to germinate and develop into seedlings. However, under abiotic stress conditions, ABA levels remain high, and growth and development are arrested. Several transcription factors, including abscisic acid‐insensitive (ABI)3 and ABI5, are known to control this developmental checkpoint. Here, we show that, in germinating Arabidopsis thaliana seeds, ABA induces the accumulation of microRNA 159 (miR159) in an ABI3‐dependent fashion, and miRNA159 mediates cleavage of MYB101 and MYB33 transcripts in vitro and in vivo . The two MYB transcription factors function as positive regulators of ABA responses, as null mutants of myb33 and myb101 show hyposensitivity to the hormone. Consistent with this, miR159 over‐expression suppresses MYB33 and MYB101 transcript levels and renders plants hyposensitive to ABA, whereas transgenic plants over‐expressing cleavage‐resistant forms of MYB33 and MYB101 are hypersensitive, as are plants over‐expressing the Turnip mosaic virus (TuMV) P1/HC‐Pro viral protein that is known to inhibit miRNA function. Our results suggest that ABA‐induced accumulation of miR159 is a homeostatic mechanism to direct MYB33 and MYB101 transcript degradation to desensitize hormone signaling during seedling stress responses.