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Exogenous 6-Benzyladenine and Kinetin Restrict Rice Seedling Root Growth, and Ag+ Partially Alleviates the Inhibition
Xiaolong Yang1, Xiaoxue Liu1,2, Bo Li1
1Hubei Key Laboratory of Food Crop Germplasm and Genetic Improvement, Institute of Food Crops, Hubei Academy of Agricultural Sciences, Wuhan 430064, China.
Abstract:
Cytokinins are key regulators of plant root development, but their dose-dependent effects on rice seedling roots and their physiological association with ethylene-related responses remain incompletely understood. In this study, rice seedlings were exposed to two exogenous cytokinins, 6-benzyladenine (6-BA) and kinetin (KT), at different concentrations for 3 and 6 d, and Ag+ was used as an inhibitor of ethylene action to evaluate its alleviating effect. Both 6-BA and KT significantly inhibited primary root elongation in a concentration- and time-dependent manner. At high cytokinin concentrations, primary root length was reduced by more than 60% relative to the control, accompanied by reductions in total root length, lateral root number, absorptive area, and root vigor, as well as increased MDA and ethylene levels. Ag+ partially alleviated cytokinin-induced primary root inhibition, with the strongest rescue effect observed near 0.08 μM. The recovery effect was particularly evident under moderate and high cytokinin concentrations. Correlation and principal component analyses further indicated that root morphological traits were negatively associated with MDA and ethylene but positively associated with root vigor. These results suggest that exogenous cytokinins restrict rice seedling root growth through a coordinated physiological response associated with ethylene accumulation and increased membrane lipid peroxidation, while Ag+ partially relieves this inhibition in association with mitigation of ethylene-related restriction. Because the study was based on short-term exogenous treatments and pharmacological inhibition, the findings should be interpreted as physiological evidence for ethylene-related involvement rather than direct proof of a complete signaling mechanism.
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