No description available.

Alternative oxidase (AOX) is a non-energy conserving branch of the mitochondrial electron transport chain (ETC) which has been hypothesized to modulate the level of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in plant mitochondria. The aim of the research presented herein is to provide direct evidence in support of this hypothesis and to explore the implications of this during plant-pathogen interactions in Nicotiana tabacum. We observed leaf levels of ROS and RNS in wild-type (Wt) tobacco and transgenic tobacco with altered AOX levels and we found that plants lacking AOX have increased levels of both NO and mitochondrial O2 - compared Wt plants. Based on the results we suggest that AOX respiration acts to reduce the generation of ROS and RNS in plant mitochondria by dampening the leak of electrons from the ETC to O2 or nitrite. We characterized multiple responses of tobacco to different pathovars of the bacterial pathogen Pseudomonas syringae. These included a compatible response associated with necrosis (pv tabaci), an incompatible response that included the hypersensitive response (HR) (pv maculicola) and an incompatible response that induced defenses (pv phaseolicola). We show that the HR is accompanied by an early mitochondrial O2 - burst prior to cell death. Also, we found iii that the appearance of HR and the appearance of the mitochondrial O2 - burst are delayed in transgenic plants lacking AOX. A similar delay is seen in transgenic plants treated with the complex III inhibitor antimycin A. In Wt plants, expression of Aox1a is suppressed during the HR response to pv maculicola despite the accumulation of signaling molecules known to induce Aox1a transcription. Also, MnSOD activity declined during the HR. We suggest that the mitochondrial ROS burst controlled by AOX and MnSOD is an important component for the induction and coordination of the HR during plant-pathogen interactions.

Age-related neurodegenerative proteinophaties, including polyglutamine (polyQ) diseases such as Huntington’s disease, are a group of disorders in which a single protein or a set of proteins misfold and aggregate resulting in a progressive and selective loss of anatomically or physiologically related neuronal systems. Despite evidence showing a clear relationship between mitochondrial dysfunction, aging and neurodegenerative proteinophaties, the extent of the mitochondrial respiratory chain deficits, the involvement of mitochondrial dysfunction and the mechanisms responsible for these processes are largely unknown. Using yeast models of cellular aging and polyQ disorders we show that mitochondrial dysfunction is an important contributor to the process of aging and age-related neurodegenerative diseases. Preserving mitochondrial function is essential for standard wild-type aging. Enhancement of mitochondrial biogenesis ameliorates polyQ cytotoxicity and is a required component of interventions that retard the aging process.

Thesis (Ph. D.)--University of Hawaii at Manoa, 1995. / Includes bibliographical references (leaves 96-106). / Microfiche. / xxii, 106 leaves, bound 29 cm

Typescript. / Bibliography: leaves 172-181. / x, 181 leaves ill

Although it has long been recognized that physiological acclimation of photosynthesis and respiration can occur in plants exposed to changing environmental conditions (e.g. light, temperature or stress), the extent of acclimation in different tissues (i.e. pre-existing and new foliage) however, has not received much attention until recently. Furthermore, few studies have investigated the extent of photosynthetic and respiratory acclimation under natural conditions, where air temperatures vary diurnally and seasonally. In this study, the effects of variations in temperature on respiratory CO2 loss and photosynthetic carbon assimilation were examined under both controlled and natural environments. The purpose of the investigations described in this thesis was to identify the effects acclimation would have on two key metabolic processes in plants exposed to temperature change, with emphasis also placed on the role of nutrition (nitrogen) and respiratory enzymatic characteristics on the potential for acclimation in two contrasting tree species, Pinus radiata and Populus deltoides. Controlled-environment studies (Chapter 2 and 3) established that rates of foliar respiration are sensitive to short-term changes in temperature (increasing exponentially with temperature) but in the longer-term (days to weeks), foliar respiration acclimates to temperature change. As a result, rates of dark respiration measured at any given temperature are higher in cold-acclimated and lower in warm-acclimated plants than would be predicted from an instantaneous response. Acclimation in new foliage (formed under the new temperature environment) was found to result in respiratory homeostasis (i.e. constant rates of foliar respiration following long-term changes in temperature, when respiration is measured at the prevailing growth temperature). Available evidence suggests that substantial adjustments in foliar respiration tend to be developmentally dependent. This may in part explain why respiratory homeostasis was only observed in new but not in pre-existing tissues. Step changes in temperature (cold and warm transfers) resulted in significant changes in photosynthetic capacity. However, in stark contrast to the findings of respiration, there was little evidence for photosynthetic acclimation to temperature change. The results obtained from field studies (Chapter 4) show that in the long-term over a full year, dark respiration rates in both tree species were insensitive to temperature but photosynthesis retained its sensitivity, increasing with increasing temperature. Respiration in both species showed a significant downregulation during spring and summer and increases in respiratory capacity were observed in autumn and winter. Thermal acclimation of respiration was associated with a change in the concentration of soluble sugars. Hence, acclimation of dark respiration under a naturally changing environment is characterized by changes in the temperature sensitivity and apparent capacity of the respiratory apparatus. The results from controlled and natural-environment studies were used to drive a leaflevel model (which accounted for dark respiratory acclimation) with the aim of forecasting the overall impact of responses of photosynthesis and respiration in the long term (Chapter 5). Modellers utilise the temperature responses of photosynthesis and respiration to parameterize carbon exchange models but often ignore acclimation and use only instantaneous responses to drive such models. The studies here have shown that this can result in erroneous estimates of carbon exchange as strong respiratory acclimation occurs over longer periods of temperature change. For example, it was found here that the failure to factor for dark respiratory acclimation resulted in the underestimation of carbon losses by foliar respiration during cooler months and an overestimation during warmer months - such discrepancies are likely to have an important impact on determinations of the carbon economy of forests and ecosystems. The overall results substantiate the conclusion that understanding the effect of variations in temperature on rates of carbon loss by plant respiration is a prerequisite for predicting estimates of atmospheric CO2 release in a changing global environment. It has been shown here that within a moderate range of temperatures, rate of carbon uptake by photosynthesis exceeds the rate of carbon loss by plant respiration in response to warming as a result of strong respiratory acclimation to temperature change. This has strong implications for models which fail to account for acclimation of respiration. At present, respiration is assumed to increase with increasing temperatures. This erroneous assumption supports conclusions linking warming to the reinforcement of the greenhouse effect.

Diss. (sammanfattning) Umeå : Univ., 2007. / Härtill 4 uppsatser.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniv., 2004. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2001. / Härtill 6 uppsatser.

Thesis (M.Sc.) --University of Adelaide, 1946. / Typewritten copy.