MIZ1-regulated hydrotropism functions in the growth and survival of Arabidopsis thaliana under natural conditions

Background and Aims

Root hydrotropism is a response to water-potential gradients that makes roots bend towards areas of higher water potential. The gene MIZU-KUSSEI1 (MIZ1) that is essential for hydrotropism in Arabidopsis roots has previously been identified. However, the role of root hydrotropism in plant growth and survival under natural conditions has not yet been proven. This study assessed how hydrotropic response contributes to drought avoidance in nature.

Methods

An experimental system was established for the study of Arabidopsis hydrotropism in soil. Characteristics of hydrotropism were analysed by comparing the responses of the miz1 mutant, transgenic plants overexpressing MIZ1 (MIZ1OE) and wild-type plants.

Key Results

Wild-type plants developed root systems in regions with higher water potential, whereas the roots of miz1 mutant plants did not show a similar response. This pattern of root distribution induced by hydrotropism was more pronounced in MIZ1OE plants than in wild-type plants. In addition, shoot biomass and the number of plants that survived under drought conditions were much greater in MIZ1OE plants.

Conclusions

These results show that hydrotropism plays an important role in root system development in soil and contributes to drought avoidance, which results in a greater yield and plant survival under water-limited conditions. The results also show that MIZ1 overexpression can be used for improving plant productivity in arid areas.     

Redundant and non-redundant roles of the trehalose-6-phosphate phosphatases in leaf growth,root hair specification and energy-responses in Arabidopsis

The Arabidopsis trehalose-6-phosphate phosphatase (TPP) gene family arose mainly from whole genome duplication events and consists of 10 genes (TPPA-J). All the members encode active TPP enzymes, possibly regulating the levels of trehalose-6-phosphate, an established signaling metabolite in plants. GUS activity studies revealed tissue-, cell- and stage-specific expression patterns for the different members of the TPP gene family. Here we list additional examples of the remarkable features of the TPP gene family. TPPA-J expression levels seem, in most of the cases, differently regulated in response to light, darkness and externally supplied sucrose. Disruption of the TPPB gene leads to Arabidopsis plants with larger leaves, which is the result of an increased cell number in the leaves. Arabidopsis TPPA and TPPG are preferentially expressed in atrichoblast cells. TPPA and TPPG might fulfill redundant roles during the differentiation process of root epidermal cells, since the tppa tppg double mutant displays a hairy root phenotype, while the respective single knockouts have a distribution of trichoblast and atrichoblast cells similar to the wild type. These new data portray redundant and non-redundant functions of the TPP proteins in regulatory pathways of Arabidopsis.     

Analysis of Vascular Development in the hydra Sterol Biosynthetic Mutants of Arabidopsis

Background

The control of vascular tissue development in plants is influenced by diverse hormonal signals, but their interactions during this process are not well understood. Wild-type sterol profiles are essential for growth, tissue patterning and signalling processes in plant development, and are required for regulated vascular patterning.

Methodology/Principal Findings

Here we investigate the roles of sterols in vascular tissue development, through an analysis of the Arabidopsis mutants hydra1 and fackel/hydra2, which are defective in the enzymes sterol isomerase and sterol C-14 reductase respectively. We show that defective vascular patterning in the shoot is associated with ectopic cell divisions. Expression of the auxin-regulated AtHB8 homeobox gene is disrupted in mutant embryos and seedlings, associated with variably incomplete vascular strand formation and duplication of the longitudinal axis. Misexpression of the auxin reporter proIAA2∶GUS and mislocalization of PIN proteins occurs in the mutants. Introduction of the ethylene-insensitive ein2 mutation partially rescues defective cell division, localization of PIN proteins, and vascular strand development.

Conclusions

The results support a model in which sterols are required for correct auxin and ethylene crosstalk to regulate PIN localization, auxin distribution and AtHB8 expression, necessary for correct vascular development.