20 research outputs found

    Seed treatments: phytotoxicity amelioration and tracer uptake

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    Seed treatments are used globally on a wide range of field, vegetable and ornamental seeds, for efficient early season control of insects and diseases. However, specific seed-treatment compounds may be phytotoxic and this phytotoxicity is most acute in laboratory germination tests. Several strategies have been developed to alleviate seed-treatment phytotoxicity that include spatial separation of the pesticide from the seed. This can be accomplished by the application of the active compounds at the end of pelleting or by using a two-pellet system, termed ‘smart-pill technology'. Another approach is to detoxify or adsorb the agrochemical in a standard germination test by applying a peat medium over the seeds in a roll towel or blotter test. Many new seed-treatment chemicals have systemic activity, and the efficacy of these systemic seed treatments depends on the ability of these applied chemical compounds to be absorbed, and then transported in the developing plant. The present article describes seed-coat permeability to systemic seed treatments, examined by monitoring the movement of fluorescent tracers into intact seeds during imbibition. Two moderately lipophilic, fluorescent tracers have been used - rhodamine (ionic) and coumarin (non-ionic) - which differ mainly in electrical charge. Seed-coat permeabilities of particular species have been grouped into three categories: (1) permeable to both tracers; (2) selectively permeable to only coumarin; and (3) non-permeable to both tracers. The ability of a particular compound to diffuse through the seed coat is related to the chemical nature of the seed-covering tissues and the physico-chemical properties of the compound applie

    Gibberellin DELLA signaling targets the retromer complex to redirect protein trafficking to the plasma membrane

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    The plant hormone gibberellic acid (GA) is a crucial regulator of growth and development. The main paradigm of GA signaling puts forward transcriptional regulation via the degradation of DELLA transcriptional repressors. GA has also been shown to regulate tropic responses by modulation of the plasma membrane incidence of PIN auxin transporters by an unclear mechanism. Here we uncovered the cellular and molecular mechanisms by which GA redirects protein trafficking and thus regulates cell surface functionality. Photoconvertible reporters revealed that GA balances the protein traffic between the vacuole degradation route and recycling back to the cell surface. Low GA levels promote vacuolar delivery and degradation of multiple cargos, including PIN proteins, whereas high GA levels promote their recycling to the plasma membrane. This GA effect requires components of the retromer complex, such as Sorting Nexin 1 (SNX1) and its interacting, microtubule (MT)-associated protein, the Cytoplasmic Linker-Associated Protein (CLASP1). Accordingly, GA regulates the subcellular distribution of SNX1 and CLASP1, and the intact MT cytoskeleton is essential for the GA effect on trafficking. This GA cellular action occurs through DELLA proteins that regulate the MT and retromer presumably via their interaction partners Prefoldins (PFDs). Our study identified a branching of the GA signaling pathway at the level of DELLA proteins, which, in parallel to regulating transcription, also target by a nontranscriptional mechanism the retromer complex acting at the intersection of the degradation and recycling trafficking routes. By this mechanism, GA can redirect receptors and transporters to the cell surface, thus coregulating multiple processes, including PIN-dependent auxin fluxes during tropic responses

    KIRA1 and ORESARA1 terminate flower receptivity by promoting cell death in the stigma of Arabidopsis

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    Flowers have a species-specific functional life span that determines the time window in which pollination, fertilization and seed set can occur. The stigma tissue plays a key role in flower receptivity by intercepting pollen and initiating pollen tube growth toward the ovary. In this article, we show that a developmentally controlled cell death programme terminates the functional life span of stigma cells in Arabidopsis. We identified the leaf senescence regulator ORESARA1 (also known as ANAC092) and the previously uncharacterized KIRA1 (also known as ANAC074) as partially redundant transcription factors that modulate stigma longevity by controlling the expression of programmed cell death-associated genes. KIRA1 expression is sufficient to induce cell death and terminate floral receptivity, whereas lack of both KIRA1 and ORESARA1 substantially increases stigma life span. Surprisingly, the extension of stigma longevity is accompanied by only a moderate extension of flower receptivity, suggesting that additional processes participate in the control of the flower's receptive life span

    Control of programmed cell death during plant reproductive development

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    Programmed cell death (PCD) is an actively controlled, genetically encoded self-destruct mechanism of the cell. While many forms of PCD have been described and molecularly dissected in animals, we know to date only little about the control of PCD processes in plants. Nevertheless, plant PCD is a crucial component of a plant’s reaction to its biotic and abiotic environment and a central theme during plant development. In this chapter, we review the communication events triggering and executing, or preventing, PCD during plant reproductive development. These comprise intracellular communication, as well as signaling between cells and tissues, and the intricate communication between genetically distinct individuals that are necessary for successful plant reproduction
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