An article entitled "The Type-B Cytokinin Response Regulator ARR1 Inhibits Shoot Regeneration in an ARR12-Dependent Manner in Arabidopsis" was published in the top journal The Plant Cell. Dr. Zhen-Hua Liu, Dr. Xue-Huan Dai, and Dr. Juan Li are the co-first authors; Prof. Feng-Ning Xiang is the corresponding author. The key laboratory of Plant Development and Environmental Adaptation Biology and School of Life Sciences are the first corresponding institutions.
In contrast to most animal cells, plant cells typically maintain totipotency, allowing regeneration of a wide variety of explant types into whole plants through the appropriate choice of in vitro culture conditions. Exogenous cytokinin is critical for in vitro shoot regeneration and media with a high cytokinin/auxin ratio are required for shoot regeneration. Some type-B ARRs (e.g., ARR1 and ARR12) promote shoot regeneration by directly activating WUSCHEL (WUS) expression. However, the functions of individual type-B ARRs in shoot regeneration are not fully understood, and the repression of shoot regeneration by type-B ARRs has not been reported.
Their study showed that ARR12 is a central enhancer of callus formation and shoot regeneration, whereas ARR1 is a strong inhibitor of this process that counteracts the positive effect of ARR12. ARR1 indirectly represses CLAVATA3 and WUS expression in an ARR12-dependent manner via competing with ARR12 for binding to their promoters, which contributes to its ARR12-dependent inhibitory effect on callus formation and shoot regeneration. In parallel, ARR1 inhibits shoot regeneration through transcriptional activation of INDOLE-3-ACETIC ACID INDUCIBLE17 (IAA17), an auxin response repressor gene, and the consequent indirect repression of WUS expression. Thus, type-B ARRs have diverse effects on callus formation and shoot regeneration. The study revealed novel molecular pathways linking cytokinin signaling, the CLV3 regulator, and auxin signaling, and shed lights on the mechanism underlying cytokinin-regulated shoot regeneration.
Prof. Xiang's group has been committed to the study of the mechanism underlying Arabidopsis shoot regeneration for years. They have identified several functional genes and miRNAs involved in shoot regeneration (The Plant Journal, 2012; 2016a; 2016b), which are conducive to the understanding of the mechanism of plant cell totipotency.
ARR1 inhibits shoot regeneration through the indirect repression of CLV3 and the direct activation of IAA17
ARR1 inhibits shoot regeneration by competing with ARR12 for binding to the WUS promoter