Browsing by Author "Kruger, L"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Item
    Restricted
    The effect of drying rate on the survival of three desiccation-tolerant angiosperm species.
    (Oxford University Press, 1999) Farrant, J; Cooper, K; Kruger, L; Sherwin, H
    The effect of drying rate on the survival of three angiosperm resurrection plants, Craterostigma wilmsii (homoiochlorophyllous), Xerophyta humilis (poikilochlorophyllous) and Myrothamnus flabellifolius (homoiochlorophyllous) was examined. All species survived slow drying, but only C. wilmsii was able to survive rapid drying. C. wilmsii was rapidly able to induce protection mechanisms such as folding of cell walls to prevent mechanical stress and curling of leaves to minimize light stress, and thus survived fast drying. Rapid drying of X. humilis andM. flabellifolius appeared to allow insufficient time for complete induction of protection mechanisms. In X. humilis, there was incomplete replacement of water in vacuoles, the photosynthetic apparatus was not dismantled, plasma membrane disruption occurred and quantum efficiency of photosystem II (FV/FM) did not recover on rehydration. Rapidly dried leaves of M. flabellifolius did not fold tightly against the stem and FV/FMdid not recover. Ultrastructural studies showed that subcellular damage incurred during drying was exacerbated on rehydration. The three species co-occur in environments in which they experience high desiccation pressures. C. wilmsii has few features to retard water loss and thus the ability for rapid induction of subcellular protection is vital to survival. X. humilis and M. flabellifolius are able to retard water loss and protection is acquired relatively slowly. Copyright 1999 Annals of Botany Company.
  • Thumbnail Image
    Item
    Restricted
    Longevity of dry Myrothamnus flabellifolius in simulated field conditions.
    (Springer, 2001) Farrant, J; Kruger, L
    This study tested the length of time the desiccation-tolerantMyrothamnus flabellifolius could remain in the dry stateunder simulated field conditions, without losing viability. Dry plants werekeptat 50% relative humidity, with a 25/16 °Cday/night temperature regime and a daylight intensity of 1200μmol·m−2 s−1. At threemonthly intervals plants were rehydrated and the ability to resume respiration,photosynthesis, protein synthesis and transcription was assessed and changes insubcellular organisation and plant growth regulator content (zeatin, zeatinriboside and abscisic acid) monitored. Plants survived in the dry state foronly one year. The ability toresurrect metabolism in existing leaves was lost after nine months, after whichsurvival occurred due to regrowth of new leaves from meristems. There waslittleevidence of subcellular damage in leaf tissues of plants kept dry for up to sixmonths. These plants recovered respiration before the onset of translation (andthus repair) suggesting considerable subcellular protection of this metabolismagainst desiccation damage. Furthermore, full recovery of metabolism, includingphotosynthesis, occurred before the onset of transcription in these plants.Somesubcellular damage occurred in plants maintained dry for nine months. There wasincreased electrolyte leakage indicative of membrane damage which was repairedwith the onset of protein synthesis. Since this repair occurred before theonsetof transcription, it is likely that stored mRNA, present in the dry leaves, wasused. Recovery of photosynthesis in plants dried for 9 months was delayed untilthe onset of transcription. We propose that mRNA for recovery of thismetabolismis not stored during drying and thus damage to the photosynthetic apparatus canbe repaired only upon de novo transcription of the genome.In leaves that were able to resurrect, cytokinin content increasedtransiently just prior to onset of chlorophyll biosynthesis and translation,andabscisic acid content increased just prior to the onset of transcription. Theseplant growth regulator changes did not occur in leaves which did not resurrect,but we cannot distinguish whether it was the lack of signal, or the extent oftissue damage (or both) which prevented the repair and recovery of metabolisminthese tissues.