Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/1/1997
Publication Date: N/A
Citation: N/A Interpretive Summary: Large areas of land within the U.S. and a significant proportion of the worlds arable lands are acidic. In these acid soils, aluminum (Al) toxicity is the primary factor limiting crop production. There is considerable genetic variation in sensitivity to Al between different plant species and genotypes, yet the genetic and molecular basis for Al tolerance is still poorly understood. We have recently screened mutagenized populations of Arabidopsis thaliana (a model plant system for molecular and genetic research) and isolated a family of mutants that exhibited increased sensitivity to Al toxicity. We showed that at least 8 different recessive genes are involved in Al sensitivity and are using these mutants to study the physiology and molecular biology of Al toxicity and tolerance in plants. In this study, we have focused on a very interesting Al sensitive mutant, als3, where Al toxicity involves disruption of shoot development (usually Al toxicity inhibits root but not shoot growth). In this study, w show that this response is specific for Al over other toxic metals, and requires Al interaction with the root and not the shoot. It appears that Al is causing a change in the root that results in dramatically inhibited shoot development, possibly via a root-derived Al-induced signal translocated to the shoot. This interesting mutant should provide new information on how Al toxicity comes about, as well as new information on developmental processes in plants.
Technical Abstract: In als3, an aluminum sensitive Arabidopsis mutant, shoot development as well as root growth is sensitive to A1. When grown in an Al-containing medium, leaf expansion as well as root growth are severely inhibited in als3 seedlings. In the presence of A1, unexpanded leaves accumulate callose, an indicator of A1 damage in roots. The possibility that the inhibition of shoot development in als3 is due to hyperaccumulation of A1 in this tissue was examined, however it was found that the levels of A1 that accumulated in shoots of als3 are not different from wild type. The inhibition of shoot development in als3 is not a consequence of non- specific damage to roots because other metals (LaCl3 or CuS04) that strongly inhibit root growth did not block shoot development in als3 seedlings. A1 did not block leaf development in excised als3 shoots grown in an Al-containing medium demonstrating that the A1 induced damage in als3 3shoots was dependent on the presence of roots. This suggests that A1 inhibition of als3 shoot development may be a delocalized response to A1- induced stresses in roots following A1 exposure.