| 1. |
- Chow, Wah Soon, et al.
(författare)
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Photoinactivation of photosystem II in leaves
- 2005
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Ingår i: Photosynthesis Research. - Dordrecht : Springer. - 0166-8595 .- 1573-5079. ; 84:1-3, s. 35-41
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Tidskriftsartikel (refereegranskat)abstract
- Photoinactivation of Photosystem II (PS II), the light-induced loss of ability to evolve oxygen, inevitably occurs under any light environment in nature, counteracted by repair. Under certain conditions, the extent of photoinactivation of PS II depends on the photon exposure (light dosage, x), rather than the irradiance or duration of illumination per se, thus obeying the law of reciprocity of irradiance and duration of illumination, namely, that equal photon exposure produces an equal effect. If the probability of photoinactivation (p) of PS II is directly proportional to an increment in photon exposure (p = kDeltax, where k is the probability per unit photon exposure), it can be deduced that the number of active PS II complexes decreases exponentially as a function of photon exposure: N = Noexp(-kx). Further, since a photon exposure is usually achieved by varying the illumination time (t) at constant irradiance (I), N = Noexp(-kI t), i.e., N decreases exponentially with time, with a rate coefficient of photoinactivation kI, where the product kI is obviously directly proportional to I. Given that N = Noexp(-kx), the quantum yield of photoinactivation of PS II can be defined as -dN/dx = kN, which varies with the number of active PS II complexes remaining. Typically, the quantum yield of photoinactivation of PS II is ca. 0.1micromol PS II per mol photons at low photon exposure when repair is inhibited. That is, when about 10(7) photons have been received by leaf tissue, one PS II complex is inactivated. Some species such as grapevine have a much lower quantum yield of photoinactivation of PS II, even at a chilling temperature. Examination of the longer-term time course of photoinactivation of PS II in capsicum leaves reveals that the decrease in N deviates from a single-exponential decay when the majority of the PS II complexes are inactivated in the absence of repair. This can be attributed to the formation of strong quenchers in severely-photoinactivated PS II complexes, able to dissipate excitation energy efficiently and to protect the remaining active neighbours against damage by light.
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| 2. |
- Hendrickson, Luke, et al.
(författare)
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Cold acclimation of the Arabidopsis dgd1 mutant results in recovery from photosystem I-limited photosynthesis.
- 2006
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Ingår i: FEBS Letters. - : Wiley. - 0014-5793. ; 580:20, s. 4959-68
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Tidskriftsartikel (refereegranskat)abstract
- We compared the thylakoid membrane composition and photosynthetic properties of non- and cold-acclimated leaves from the dgd1 mutant (lacking >90% of digalactosyl–diacylglycerol; DGDG) and wild type (WT) Arabidopsis thaliana. In contrast to warm grown plants, cold-acclimated dgd1 leaves recovered pigment-protein pools and photosynthetic function equivalent to WT. Surprisingly, this recovery was not correlated with an increase in DGDG. When returned to warm temperatures the severe dgd1 mutant phenotype reappeared. We conclude that the relative recovery of photosynthetic activity at 5 °C resulted from a temperature/lipid interaction enabling the stable assembly of PSI complexes in the thylakoid.
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| 3. |
- Ivanov, Alexander G, et al.
(författare)
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Digalactosyl-diacylglycerol deficiency impairs the capacity for photosynthetic intersystem electron transport and state transitions in Arabidopsis thaliana due to photosystem I acceptor-side limitations.
- 2006
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Ingår i: Plant Cell Physiology. - : Oxford University Press (OUP). - 0032-0781 .- 1471-9053. ; 47:8, s. 1146-57
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Tidskriftsartikel (refereegranskat)abstract
- Compared with wild type, the dgd1 mutant of Arabidopsis thaliana exhibited a lower amount of PSI-related Chl–protein complexes and lower abundance of the PSI-associated polypeptides, PsaA, PsaB, PsaC, PsaL and PsaH, with no changes in the levels of Lhca1–4. Functionally, the dgd1 mutant exhibited a significantly lower light-dependent, steady-state oxidation level of P700 (P700+) in vivo, a higher intersystem electron pool size, restricted linear electron transport and a higher rate of reduction of P700+ in the dark, indicating an increased capacity for PSI cyclic electron transfer compared with the wild type. Concomitantly, the dgd1 mutant exhibited a higher sensitivity to and incomplete recovery of photoinhibition of PSI. Furthermore, dgd1 exhibited a lower capacity to undergo state transitions compared with the wild type, which was associated with a higher reduction state of the plastoquinone (PQ) pool. We conclude that digalactosyl-diacylglycerol (DGDG) deficiency results in PSI acceptor-side limitations that alter the flux of electrons through the photosynthetic electron chain and impair the regulation of distribution of excitation energy between the photosystems. These results are discussed in terms of thylakoid membrane domain reorganization in response to DGDG deficiency in A. thaliana.
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| 4. |
- Kleine, Tatjana, et al.
(författare)
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Genome-wide gene expression analysis reveals a critical role for CRYPTOCHROME1 in the response of Arabidopsis to high irradiance
- 2007
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Ingår i: Plant Physiology. - : Oxford University Press (OUP). - 0032-0889 .- 1532-2548. ; 144:3, s. 1391-406
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Tidskriftsartikel (refereegranskat)abstract
- Exposure to high irradiance results in dramatic changes in nuclear gene expression in plants. However, little is known about the mechanisms by which changes in irradiance are sensed and how the information is transduced to the nucleus to initiate the genetic response. To investigate whether the photoreceptors are involved in the response to high irradiance, we analyzed expression of EARLY LIGHT-INDUCIBLE PROTEIN1 (ELIP1), ELIP2, ASCORBATE PEROXIDASE2 (APX2), and LIGHT-HARVESTING CHLOROPHYLL A/B-BINDING PROTEIN2.4 (LHCB2.4) in the phytochrome A (phyA), phyB, cryptochrome1 (cry1), and cry2 photoreceptor mutants and long hypocotyl5 (hy5) and HY5 homolog (hyh) transcription factor mutants. Following exposure to high intensity white light for 3 h (1,000 µmol quanta m–2 s–1) expression of ELIP1/2 and APX2 was strongly induced and LHCB2.4 expression repressed in wild type. The cry1 and hy5 mutants showed specific misregulation of ELIP1/2, and we show that the induction of ELIP1/2 expression is mediated via CRY1 in a blue light intensity-dependent manner. Furthermore, using the Affymetrix Arabidopsis (Arabidopsis thaliana) 24 K Gene-Chip, we showed that 77 of the high light-responsive genes are regulated via CRY1, and 26 of those genes were also HY5 dependent. As a consequence of the misregulation of these genes, the cry1 mutant displayed a high irradiance-sensitive phenotype with significant photoinactivation of photosystem II, indicated by reduced maximal fluorescence ratio. Thus, we describe a novel function of CRY1 in mediating plant responses to high irradiances that is essential to the induction of photoprotective mechanisms. This indicates that high irradiance can be sensed in a chloroplast-independent manner by a cytosolic/nucleic component.
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| 5. |
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| 6. |
- Rosso, Dominic, et al.
(författare)
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IMMUTANS does not act as a stress-induced safety valve in the protection of the photosynthetic apparatus of Arabidopsis during steady-state photosynthesis.
- 2006
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Ingår i: Plant Physiology. - : Oxford University Press (OUP). - 0032-0889 .- 1532-2548. ; 142:2, s. 574-85
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Tidskriftsartikel (refereegranskat)abstract
- IMMUTANS (IM) encodes a thylakoid membrane protein that has been hypothesized to act as a terminal oxidase that couples the reduction of O2 to the oxidation of the plastoquinone (PQ) pool of the photosynthetic electron transport chain. Because IM shares sequence similarity to the stress-induced mitochondrial alternative oxidase (AOX), it has been suggested that the protein encoded by IM acts as a safety valve during the generation of excess photosynthetically generated electrons. We combined in vivo chlorophyll fluorescence quenching analyses with measurements of the redox state of P700 to assess the capacity of IM to compete with photosystem I for intersystem electrons during steady-state photosynthesis in Arabidopsis (Arabidopsis thaliana). Comparisons were made between wild-type plants, im mutant plants, as well as transgenics in which IM protein levels had been overexpressed six (OE-6x) and 16 (OE-16x) times. Immunoblots indicated that IM abundance was the only major variant that we could detect between these genotypes. Overexpression of IM did not result in increased capacity to keep the PQ pool oxidized compared to either the wild type or im grown under control conditions (25°C and photosynthetic photon flux density of 150 µmol photons m–2 s–1). Similar results were observed either after 3-d cold stress at 5°C or after full-leaf expansion at 5°C and photosynthetic photon flux density of 150 µmol photons m–2 s–1. Furthermore, IM abundance did not enhance protection of either photosystem II or photosystem I from photoinhibition at either 25°C or 5°C. Our in vivo data indicate that modulation of IM expression and polypeptide accumulation does not alter the flux of intersystem electrons to P700+ during steady-state photosynthesis and does not provide any significant photoprotection. In contrast to AOX1a, meta-analyses of published Arabidopsis microarray data indicated that IM expression exhibited minimal modulation in response to myriad abiotic stresses, which is consistent with our functional data. However, IM exhibited significant modulation in response to development in concert with changes in AOX1a expression. Thus, neither our functional analyses of the IM knockout and overexpression lines nor meta-analyses of gene expression support the model that IM acts as a safety valve to regulate the redox state of the PQ pool during stress and acclimation. Rather, IM appears to be strongly regulated by developmental stage of Arabidopsis.
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