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Reduced root meristem length in tic mutant is due to the repressed expression of PIN genes for decreased acropetal auxin transport, leading to low auxin accumulation. MYC2-mediated JA-signaling pathway may not be involved in this processRoots play important roles in plant survival and productivity as they not only anchor the plants in the soil but are also the primary organ for the uptake of nutrients from the outside. The growth and development of roots depend on the specification and maintenance of the root meristem. Here, we report a previously unknown role of TIME FOR COFFEE (TIC) in controlling root meristem size in Arabidopsis. The results showed that loss of function of TIC reduced root meristem length and cell number by decreasing the competence of meristematic cells to divide. This was due to the repressed expression of PIN genes for decreased acropetal auxin transport in tic-2, leading to low auxin accumulation in the roots responsible for reduced root meristem, which was verified by exogenous application of indole-3-acetic acid. Downregulated expression of PLETHORA1 (PLT1) and PLT2, key transcription factors in mediating the patterning of the root stem cell niche, was also assayed in tic-2. Similar results were obtained with tic-2 and wild-type plants at either dawn or dusk. We also suggested that the MYC2-mediated jasmonic acid signalling pathway may not be involved in the regulation of TIC in controlling the root meristem. Taken together, these results suggest that TIC functions in an auxin–PLTs loop for maintenance of post-embryonic root meristem. [ABSTRACT FROM PUBLISHER]

Aux/IAAs interact with auxin response factors (ARFs) to repress their transcriptional activity in the auxin signaling pathway. Previous studies have focused on gain-of-function mutations of domain II and little is known about whether the expression level of wild-type Aux/IAAs can modulate auxin homeostasis. Here we examined the perturbation of auxin homeostasis by ectopic expression of wild-type IAA15. Root gravitropism and stem cell differentiation were also analyzed. The transgenic lines were less sensitive to exogenous auxin and exhibited low-auxin phenotypes including failures in gravity response and defects in stem cell differentiation. Overexpression lines also showed an increase in auxin concentration and reduced polar auxin transport. These results demonstrate that an alteration in the expression of wild-type IAA15 can disrupt auxin homeostasis. [ABSTRACT FROM AUTHOR]