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81.
82.
Oxygen Requirement and Inhibition of C4
Photosynthesis
: An Analysis of C4 Plants Deficient in the
C3 and C4 Cycles 总被引:2,自引:0,他引:2
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Jo?o P. Maroco Maurice S.B. Ku Peter J. Lea Louisa V. Dever Richard C. Leegood Robert T. Furbank Gerald E. Edwards 《Plant physiology》1998,116(2):823-832
The basis for O2 sensitivity of C4 photosynthesis was evaluated using a C4-cycle-limited mutant of Amaranthus edulis (a phosphoenolpyruvate carboxylase-deficient mutant), and a C3-cycle-limited transformant of Flaveria bidentis (an antisense ribulose-1,5-bisphosphate carboxylase/oxygenase [Rubisco] small subunit transformant). Data obtained with the C4-cycle-limited mutant showed that atmospheric levels of O2 (20 kPa) caused increased inhibition of photosynthesis as a result of higher levels of photorespiration. The optimal O2 partial pressure for photosynthesis was reduced from approximately 5 kPa O2 to 1 to 2 kPa O2, becoming similar to that of C3 plants. Therefore, the higher O2 requirement for optimal C4 photosynthesis is specifically associated with the C4 function. With the Rubisco-limited F. bidentis, there was less inhibition of photosynthesis by supraoptimal levels of O2 than in the wild type. When CO2 fixation by Rubisco is limited, an increase in the CO2 concentration in bundle-sheath cells via the C4 cycle may further reduce the oxygenase activity of Rubisco and decrease the inhibition of photosynthesis by high partial pressures of O2 while increasing CO2 leakage and overcycling of the C4 pathway. These results indicate that in C4 plants the investment in the C3 and C4 cycles must be balanced for maximum efficiency. 相似文献
83.
Louisa V. Dever Mark Pearson Robert J. Ireland Richard C. Leegood Peter J. Lea 《Planta》1998,206(4):649-656
A mutant of Amaranthus edulis (Speg.) lacking activity of the C4 leaf form of NAD-malic enzyme (ME; EC 1.1.1.39) has been isolated. Homozygous mutant (5% wild-type ME activity) and heterozygous
(50% wild-type ME activity) F2 plants were shown to contain both the α and β NAD-ME subunits in similar amounts to those detected in the wild-type leaves.
The rate of photosynthetic CO2 assimilation was reduced in the homozygous mutant to 5% of that observed for the wild-type leaves. Other C4 enzymes were not down-regulated in the mutant plants. There was little difference in photosynthetic rate of the heterozygous
plants compared to the wild-type, suggesting that NAD-ME exerts little control over the rate of C4 photosynthesis, and that in the wild-type the enzyme has a very low control coefficient. The activity loss in the heterozygote
may therefore be compensated by regulatory mechanisms that increase the activity of the enzyme in vivo. Data for bundle-sheath
strands indicated that although the homozygous mutants were able to oxidise malate via the Krebs cycle, they were unable to
convert malate to pyruvate and alanine via NAD-ME.
Received: 2 April 1998 / Accepted: 7 May 1998 相似文献
84.
Daniel Bronder Anthony Tighe Darawalee Wangsa Dali Zong Thomas J. Meyer Ren Wardenaar Paul Minshall Daniela Hirsch Kerstin Heselmeyer-Haddad Louisa Nelson Diana Spierings Joanne C. McGrail Maggie Cam Andr Nussenzweig Floris Foijer Thomas Ried Stephen S. Taylor 《Disease models & mechanisms》2021,14(11)
85.
Insulin has been shown to acutely regulate hepatic apolipoprotein B (apoB) secretion at both translational and post-translational levels; however, mechanisms of apoB mRNA translational control are largely unknown. Recent studies of apoB untranslated regions (UTRs) revealed a potentially important role for cis-trans interactions at the 5' and 3' UTRs. In the present paper, deletion constructs of the UTR regions of apoB revealed that the 5' UTR was necessary and sufficient for insulin to inhibit synthesis of apoB15. Metabolic radiolabeling and in vitro translation experiments in the presence of protease inhibitors confirmed that the effect of insulin on the apoB 5' UTR was translational in nature. Using the nondenaturing electrophoretic mobility shift assay (EMSA), protein-RNA complexes were detected binding to the apoB 5' and 3' UTRs. Denaturing EMSA identified a 110-kDa protein interacting at the 5' UTR. Nondenaturing EMSA determined that insulin altered binding of large protein complexes to the 5' UTR. Binding specificity was determined by competition with both specific and nonspecific competitors. Insulin treatment decreased binding of the 110-kDa protein to the 5' UTR as visualized by EMSA. Absence of insulin increased binding of this trans-acting factor to the 5' UTR by 2-fold. Analysis of the 3' UTR showed no significant insulin-mediated changes in binding of trans-acting factors. We thus propose the existence of a novel RNA-binding insulin-sensitive factor that binds to the 5' UTR and may regulate apoB mRNA translation. Perturbations in hepatic insulin signaling as observed in insulin-resistant states may alter cis-trans interactions at the 5' UTR, leading to alterations in the rate of apoB mRNA translation, thus contributing to apoB-lipoprotein overproduction. 相似文献
86.
Light, the circadian clock, and sugar perception in the control of lignin biosynthesis 总被引:10,自引:0,他引:10
Rogers LA Dubos C Cullis IF Surman C Poole M Willment J Mansfield SD Campbell MM 《Journal of experimental botany》2005,56(416):1651-1663
88.
Drosophila Nedd4, a ubiquitin ligase,is recruited by Commissureless to control cell surface levels of the roundabout receptor 总被引:5,自引:0,他引:5
Crossing the midline produces changes in axons such that they are no longer attracted to the midline. In Drosophila, Roundabout reaches high levels on axons once they have crossed the midline, and this prohibits recrossing. Roundabout protein levels are regulated by Commissureless. We show that Commissureless binds to and is regulated by the ubiquitin ligase DNedd4. We further show that the ability of Commissureless to regulate Roundabout protein levels requires an intact DNedd4 binding site and ubiquitin acceptor sites within the Commissureless protein. The ability of Commissureless to regulate Robo in the embryo also requires a Commissureless/DNedd4 interaction. Our results show that changes in axonal sensitivity to external cues during pathfinding across the midline makes use of ubiquitin-dependent mechanisms to regulate transmembrane protein levels. 相似文献
89.
Alzheimer's disease may arise from or produce oxidative damage in the brain. To assess the responses of the Alzheimer's brain to possible oxidative challenges, we assayed for glutathione, glucose-6-phosphate dehydrogenase, catalase and superoxide dismutase in twelve regions of Alzheimer's disease and aged control brains. In addition, we determined levels of malondialdehyde to evaluate lipid peroxidation in these brain regions. Most brain regions showed evidence of a response to an oxidative challenge, but the cellular response to this challenge differed among brain regions. These data suggest that the entire Alzheimer's brain may be subject to an oxidative challenge, but that some brain areas may be more vulnerable than others to the consequent neural damage that characterizes the disease. 相似文献
90.
Crispin T. Hiley Louisa S. Chard Rathi Gangeswaran James R. Tysome Arnaud Briat Nicholas R. Lemoine Yaohe Wang 《Journal of virology》2013,87(5):2781-2790
Vaccinia virus (VV) is an enveloped DNA virus from the poxvirus family and has played a crucial role in the eradication of smallpox. It continues to be used in immunotherapy for the prevention of infectious diseases and treatment of cancer. However, the mechanisms of poxvirus entry, the host factors that affect viral virulence, and the reasons for its natural tropism for tumor cells are incompletely understood. By studying the effect of hypoxia on VV infection, we found that vascular endothelial growth factor A (VEGF-A) augments oncolytic VV cytotoxicity. VEGF derived from tumor cells acts to increase VV internalization, resulting in increased replication and cytotoxicity in an AKT-dependent manner in both tumor cells and normal respiratory epithelial cells. Overexpression of VEGF also enhances VV infection within tumor tissue in vivo after systemic delivery. These results highlight the importance of VEGF expression in VV infection and have potential implications for the design of new strategies to prevent poxvirus infection and the development of future generations of oncolytic VV in combination with conventional or biological therapies. 相似文献