Background
The plant growth retardant mepiquat chloride (MC) has been extensively used to produce compact plant canopies and increase yield in cotton (Gossypium hirsutum L.). Previous studies mainly focused on the role of gibberellins (GA) in MC-induced growth inhibition of cotton. However, the molecular mechanism underlying MC-induced growth retardation has remained largely unknown.
Results
In the present study, we conducted histological, transcriptomic, and phytohormone analyses of the second elongating internodes of cotton seedlings treated with MC. Histological analysis revealed that the MC-mediated shortening of internodes was caused by the suppression of cell division and decrease in cell length; this phenotype was confirmed by transcriptome profiling. Many genes related to cell growth were significantly downregulated in MC-treated internodes, such as cell cycle, cell wall biosynthesis and modification, and transport protein aquaporins. Furthermore, the expression of genes related to secondary metabolism, especially lignin and flavonoid, was down-regulated by MC treatment. The expression of genes related to GA, auxin, brassinosteroid (BR), and ethylene metabolism and signaling was remarkably suppressed, whereas that of genes related to cytokinin (CK) and abscisic acid (ABA) metabolism was induced by MC. Consistent with RNA-Seq analysis, significant decrease in endogenous GA, auxin, and BR content, but an increase in CK content, was observed in cotton internodes after MC treatment. In addition, many transcription factors (TFs) such as bHLH, AP2-EREBP, Orphans, MYB, GRF, and TCP were differentially regulated by MC; these TFs are associated with cell division and expansion, phytohormone signaling, and circadian rhythm.
Conclusions
This study provides novel insights into the molecular mechanism underlying the MC-mediated inhibition of internode elongation in cotton seedlings. MC reduces internode elongation by suppressing the biosynthesis and downstream signaling cascades of GA, auxin, and BR; altering the expression of many TFs; and further reducing cell division and expansion.