Long-standing models propose that plant growth responses to light or gravity are mediated by asymmetric distribution of the phytohormone auxin 1 -3 . Physiological studies implicated a specific transport system that relocates auxin laterally, thereby effecting differential growth 4 ; however, neither the molecular components of this system nor the cellular mechanism of auxin redistribution on light or gravity perception have been identified. Here, we show that auxin accumulates asymmetrically during differential growth in an efflux-dependent manner. Mutations in the Arabidopsis gene PIN3, a regulator of auxin efflux, alter differential growth. PIN3 is expressed in gravity-sensing tissues, with PIN3 protein accumulating predominantly at the lateral cell surface. PIN3 localizes to the plasma membrane and to vesicles that cycle in an actin-dependent manner. In the root columella, PIN3 is positioned symmetrically at the plasma membrane but rapidly relocalizes laterally on gravity stimulation. Our data indicate that PIN3 is a component of the lateral auxin transport system regulating tropic growth. In addition, actin-dependent relocalization of PIN3 in response to gravity provides a mechanism for redirecting auxin flux to trigger asymmetric growth.Plants orientate their growth with respect to the direction of light (phototropism) or gravity (gravitropism)1 . As early as 1926 a widely accepted model for plant tropisms, the Cholodny -Went hypothesis, was presented 2 . It proposes differential distribution of the plant hormone auxin in lateral direction on gravity or light stimulation. Subsequently, different auxin levels elicit differential growth rates, which ultimately lead to bending of the shoot or root 3 . Visualization of asymmetrically distributed auxin response in gravistimulated tobacco stems 5 and Arabidopsis roots 6 experimentally supported this hypothesis. Polar auxin transport represent a plausible means of lateral auxin distribution, as its chemical inhibition affects differential growth responses such as tropisms and apical hook formation 7,8 . Physiologically characterized components of polar auxin transport are cellular efflux carriers, whose polar localization within cells is thought to determine the direction of auxin flux 9 . The recently identified PIN genes of Arabidopsis appear to encode essential components of these carriers 7 . A role of PIN2 in regulation of basipetal auxin transport and gravitropism in root 6,10,11 as well as a role of PIN1 in basipetal auxin transport in the stem have been reported 12 ; however, so far the molecular basis of shoot tropic responses remains elusive. Lateral auxin transport with a specific, laterally localized auxin efflux carrier was proposed 4 to explain the exchange of auxin between vasculature, where the main basipetal auxin stream occurs 13 , and peripheral tissues controlling elongation 14 . Nevertheless the lack of any molecular data supporting this concept still leaves the existence of such a system in question.We analysed the relationship between auxi...
Polar auxin transport controls multiple developmental processes in plants, including the formation of vascular tissue. Mutations affecting the PIN-FORMED (PIN1) gene diminish polar auxin transport in Arabidopsis thaliana inflorescence axes. The AtPIN1 gene was found to encode a 67-kilodalton protein with similarity to bacterial and eukaryotic carrier proteins, and the AtPIN1 protein was detected at the basal end of auxin transport–competent cells in vascular tissue. AtPIN1 may act as a transmembrane component of the auxin efflux carrier.
Biotrophic plant pathogenic fungi differentiate specialized infection structures within the living cells of their host plants. These haustoria have been linked to nutrient uptake ever since their discovery. We have for the first time to our knowledge shown that the flow of sugars from the host Vicia faba to the rust fungus Uromyces fabae seems to occur largely through the haustorial complex. One of the most abundantly expressed genes in rust haustoria, the expression of which is negligible in other fungal structures, codes for a hexose transporter. Functional expression of the gene termed HXT1 in Saccharomyces cerevisiae and Xenopus laevis oocytes assigned a substrate specificity for D-glucose and D-fructose and indicated a proton symport mechanism. Abs against HXT1p exclusively labeled haustoria in immunofluorescence microscopy and the haustorial plasma membrane in electron microscopy. These results suggest that the fungus concentrates this transporter in haustoria to take advantage of a specialized compartment of the haustorial complex. The extrahaustorial matrix, delimited by the plasma membranes of both host and parasite, constitutes a newly formed apoplastic compartment with qualities distinct from those of the bulk apoplast. This organization might facilitate the competition of the parasite with natural sink organs of the host.
To exploit plants as living substrates, biotrophic fungi have evolved remarkable variations of their tubular cells, the hyphae. They form infection structures such as appressoria, penetration hyphae and infection hyphae to invade the plant with minimal damage to host cells. To establish compatibility with the host, controlled secretory activity and distinct interface layers appear to be essential. Colletotrichum species switch from initial biotrophic to necrotrophic growth and are amenable to mutant analysis and molecular studies. Obligate biotrophic rust fungi can form the most specialized hypha: the haustorium. Gene expression and immunocytological studies with rust fungi support the idea that the haustorium is a transfer apparatus for the long-term absorption of host nutrients.
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