Abstract
Auxin-induced cell elongation relies in part on the acidification of the cell wall, a process known as acid growth that presumably triggers expansin-mediated wall loosening via altered interactions between cellulose microfibrils. Cellulose microfibrils are a major determinant for anisotropic growth and they provide the scaffold for cell wall assembly. Little is known about how acid growth depends on cell wall architecture. To explore the relationship between acid growth-mediated cell elongation and plant cell wall architecture, two mutants (jia1-1 and csi1-3) that are defective in cellulose biosynthesis and cellulose microfibril organization were analyzed. The study revealed that cell elongation is dependent on CSI1-mediated cell wall architecture but not on the overall crystalline cellulose content. We observed a correlation between loss of crossed-polylamellate walls and loss of auxin- and fusicoccin-induced cell growth in csi1-3. Furthermore, induced loss of crossed-polylamellate walls via disruption of cortical microtubules mimics the effect of csi1 in acid growth. We hypothesize that CSI1- and microtubule-dependent crossed-polylamellate walls are required for acid growth in Arabidopsis hypocotyls.
Highlights
Anisotropic cell expansion is a characteristic feature of plant cells
Crossed-polylamellate walls are often observed in rapidly growing epidermal cells in both hypocotyls and roots (Chafe and Wardrop, 1972; Hodick and Kutschera, 1992; Roland et al, 1977; Takeda and Shibaoka, 1981)
It is postulated that different mechanisms account for crossed-polylamellate wall feature in two systems (Li et al, 2014)
Summary
Anisotropic cell expansion is a characteristic feature of plant cells. Plant cells respond to developmental and environmental stimuli by altering the growth direction. The inhibition of elongation in procuste, a cellulose synthase mutant of Arabidopsis, was accompanied by normal deposition of transverse orientation of nascent cellulose microfibrils in hypocotyl epidermal cell wall (MacKinnon et al, 2006). Early studies are limited by failure to observe dynamic reorganization of cellulose microfibrils as inferred by visualization of CESA trajectories (Chan et al, 2010). To add another layer of complexity, the alignment of cellulose microfibrils at the inner and outer periclinal walls of epidermal cells differs significantly (Supplementary Fig. S1)
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