Abstract
The control of cellular growth is central to multicellular patterning. In plants, the encapsulating cell wall literally binds neighbouring cells to each other and limits cellular sliding/migration. In contrast to its developmental importance, growth regulation is poorly understood in plants. Here, we reveal that the phytohormone auxin impacts on the shape of the biggest plant organelle, the vacuole. TIR1/AFBs-dependent auxin signalling posttranslationally controls the protein abundance of vacuolar SNARE components. Genetic and pharmacological interference with the auxin effect on vacuolar SNAREs interrelates with auxin-resistant vacuolar morphogenesis and cell size regulation. Vacuolar SNARE VTI11 is strictly required for auxin-reliant vacuolar morphogenesis and loss of function renders cells largely insensitive to auxin-dependent growth inhibition. Our data suggests that the adaptation of SNARE-dependent vacuolar morphogenesis allows auxin to limit cellular expansion, contributing to root organ growth rates.
Highlights
Symplastic growth, characterised by cells that do not alter their relative position to each other, is typical in plant tissue expansion (Priestley, 1930; Erickson, 1986)
We hypothesised that if the vacuolar morphology contributes to cellular size, the growth regulator auxin may impact on its regulation
It has been noted that the morphology of plant vacuoles correlate with cell size (Owens and Poole, 1979; Berger et al, 1998; Lofke et al, 2013) and, it was tempting to postulate that vacuoles may even drive cellular growth (Marty, 1999)
Summary
Symplastic growth, characterised by cells that do not alter their relative position to each other, is typical in plant tissue expansion (Priestley, 1930; Erickson, 1986) Such development implies supracellular (above the level of single cells) regulation, which has an enormous impact on cellular growth control for plant patterning. Despite their importance, molecular mechanisms that restrict cellular and tissue growth are poorly understood in plants. Auxin-dependent formation of such a co-receptor pair triggers the ubiquitination and subsequent degradation of Aux/ IAA proteins. Auxin-dependent Aux/IAA degradation leads to the release of ARF transcription factors and subsequent transcriptional responses (for reviews, see Quint and Gray, 2006; Sauer et al, 2013)
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