Root gravitropism requires lateral root cap and epidermal cells for transport and response to a mobile auxin signal

Multiscale modelling of auxin transport in the plant-root elongation zone

“…in the rootward direction) in the centre of the root and in an upwards (shootward) direction though the root's outer layers. The flux through the root's outer layers is important in producing a gravitropic response (Rashotte et al 2000;Swarup et al 2005): if the root is not orientated downwards (in the direction of gravity) the columella cells, located at the root tip, create a lateral auxin gradient (Ottenschlager et al 2003); due to the upward flux though the root's outer layers, the elongation-zone cells on the underside of the root receive more auxin than those on the upper side, which causes them to reduce their elongation rate; within minutes, this process causes the root to bend and reorientate in the direction of gravity (Friml 2003;Swarup et al 2005;Tanaka et al 2006).…”

“…On the cortical cell membranes, the location of the PIN1 and PIN2 carriers is currently unclear, with some sources reporting a rootward location (Blilou et al 2005) and others a shootward one (Peer et al 2004). There are also spatial variations in the AUX1 influx carriers, these being present on all sides of the epidermal cell membranes, but not on the cortical and endodermal cell membranes (Swarup et al 2005). With this spatial distribution, the carriers create a shootward auxin flux in the outer layers of the elongation zone that balances the rootward flux through the root centre (Blilou et al 2005;Friml et al 2002).…”

“…With this spatial distribution, the carriers create a shootward auxin flux in the outer layers of the elongation zone that balances the rootward flux through the root centre (Blilou et al 2005;Friml et al 2002). In Arabidoposis thaliana, various mutants demonstrate the importance of the carriers; for example, both aux1 and pin2 mutants (which have dysfunctional AUX1 carriers and PIN2 carriers, respectively) have disrupted auxin transport and are agravitropic (Rashotte et al 2000;Swarup et al 2005). Such mutations will be explored within our model framework below.…”

“…The labels C, F, K, and M are provided to clarify the discussion in Sect. 2 Swarup et al 2005), vein formation (Feugier et al 2005;Feugier and Iwasa 2006;Merks et al 2007;Mitchison 1980a;Mitchison et al 1981;Rolland-Lagan and Prusinkiewicz 2005) and organ initiation (de Reuille et al 2006;Heisler and Jönsson 2006;Jönsson et al 2006;Laskowski et al 2008;Stoma et al 2008;Newell et al 2008;Perrine-Walker et al 2010;Smith et al 2006;Stoma et al 2008), for example. Early studies (Goldsmith et al 1981;Martin et al 1990;Mitchison 1980b) considered only a single line of cells, with auxin diffusion within the cytoplasms and with passive and carrier-mediated transport across the cell membranes; these showed how the efflux carriers increase the tissue-scale auxin flux.…”

“…Early studies (Goldsmith et al 1981;Martin et al 1990;Mitchison 1980b) considered only a single line of cells, with auxin diffusion within the cytoplasms and with passive and carrier-mediated transport across the cell membranes; these showed how the efflux carriers increase the tissue-scale auxin flux. More recent studies have considered more complex tissue geometries and have incorporated apoplastic diffusion Jönsson et al 2006;Kramer 2004;Laskowski et al 2008;Swarup et al 2005), saturable carrier-mediated transport (de Reuille et al 2006;Feugier et al 2005;Jönsson et al 2006;Merks et al 2007;Smith et al 2006), cytoplasmic structure (Kramer 2004;Perrine-Walker et al 2010), cell growth (Chavarrıa-Krauser et al 2005;Grieneisen et al 2007;Jönsson et al 2006;Mironova et al 2010;Stoma et al 2008), auxin production and degradation (Feugier and Iwasa 2006;Feugier et al 2005;Perrine-Walker et al 2010;Heisler and Jönsson 2006;Jönsson et al 2006;Smith et al 2006;Stoma et al 2008) and dynamics of the efflux carriers Jönsson et al 2006;Kramer 2009;Merks et al 2007;Mironova et al 2010;Stoma et al 2008).…”