Regulatory network of miRNA/mRNA by miR-168a-mediated SlAGO1 and K+ deficiency stress tolerance
Based on analysis of miRNAs and mRNAs responding to K+deficiency stress, we developed a model of miR-168 -mediated AGO1 function in low K+ tolerance (Fig. 9). SlAGO1is regulated by SlmiR-168a in response to K+deficiency stress, and SlAGO1 protein then induces the expression of miR-530 , miR-384 , miR-858 , andPC-3p-276756_24 , resulting in inhibition of the targets of these miRNAs, which participate in CTK signalling. SlAGO1 also inducesmiR-171 expression and downregulates its targets, which are involved in root epidermal cell differentiation. Moreover,SlmiR-168a -mediated SlAGO1 regulates the expression ofmiR-8007 , which is involved in the ABA signalling pathway; Ca2+ may have functions in this pathway as well.
Overall, our findings demonstrated that SlmiR-168a mediatedSlAGO1 expression in response to K+ deficiency stress, resulting in modulation of root growth and CTK/ABA signalling. Other hormonal or regulatory pathways may be involved as well, necessitating further studies. However, our results clearly revealed the new roles of SlmiR-168a -mediated SlAGO1 in the response to low K+ stress and highlighted the importance ofSlAGO1 in maintaining the homeostasis of miRNA accumulation. Although further studies are needed to elucidate the detailed mechanisms of the miRNA targets mediated by low K+ stress responses, our study provided important insights into plant stress regulatory pathways and improved our understanding ofmiR-168 -mediated AGO1 function in response to low K+.