Interaction between plastid and mitochondrial retrograde signalling pathways during changes to plastid redox status. Blanco, N. E., Guinea-Díaz, M., Whelan, J., & Strand, Å. Philosophical Transactions of the Royal Society B: Biological Sciences, 369(1640):20130231, April, 2014. ![Interaction between plastid and mitochondrial retrograde signalling pathways during changes to plastid redox status [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex 1 download Mitochondria and chloroplasts depend upon each other; photosynthesis provides substrates for mitochondrial respiration and mitochondrial metabolism is essential for sustaining photosynthetic carbon assimilation. In addition, mitochondrial respiration protects photosynthesis against photoinhibition by dissipating excess redox equivalents from the chloroplasts. Genetic defects in mitochondrial function result in an excessive reduction and energization of the chloroplast. Thus, it is clear that the activities of mitochondria and plastids need to be coordinated, but the manner by which the organelles communicate to coordinate their activities is unknown. The regulator of alternative oxidase ( rao1) mutant was isolated as a mutant unable to induce AOX1a expression in response to the inhibitor of the mitochondrial cytochrome c reductase (complex III), antimycin A. RAO1 encodes the nuclear localized cyclin-dependent kinase E1 (CDKE1). Interestingly, the rao1 mutant demonstrates a genome uncoupled phenotype also in response to redox changes in the photosynthetic electron transport chain. Thus, CDKE1 was shown to regulate both LIGHT HARVESTING COMPLEX B ( LHCB ) and ALTERNATIVE OXIDASE 1 ( AOX1a ) expression in response to retrograde signals. Our results suggest that CDKE1 is a central nuclear component integrating mitochondrial and plastid retrograde signals and plays a role in regulating energy metabolism during the response to stress.
@article{blanco_interaction_2014,
title = {Interaction between plastid and mitochondrial retrograde signalling pathways during changes to plastid redox status},
volume = {369},
issn = {0962-8436, 1471-2970},
url = {https://royalsocietypublishing.org/doi/10.1098/rstb.2013.0231},
doi = {10/f226pk},
abstract = {Mitochondria and chloroplasts depend upon each other; photosynthesis provides substrates for mitochondrial respiration and mitochondrial metabolism is essential for sustaining photosynthetic carbon assimilation. In addition, mitochondrial respiration protects photosynthesis against photoinhibition by dissipating excess redox equivalents from the chloroplasts. Genetic defects in mitochondrial function result in an excessive reduction and energization of the chloroplast. Thus, it is clear that the activities of mitochondria and plastids need to be coordinated, but the manner by which the organelles communicate to coordinate their activities is unknown. The
regulator of alternative oxidase
(
rao1)
mutant was isolated as a mutant unable to induce
AOX1a
expression in response to the inhibitor of the mitochondrial cytochrome
c
reductase (complex III), antimycin A.
RAO1
encodes the nuclear localized cyclin-dependent kinase E1 (CDKE1). Interestingly, the
rao1
mutant demonstrates a genome uncoupled phenotype also in response to redox changes in the photosynthetic electron transport chain. Thus, CDKE1 was shown to regulate both
LIGHT HARVESTING COMPLEX B
(
LHCB
) and
ALTERNATIVE OXIDASE 1
(
AOX1a
) expression in response to retrograde signals. Our results suggest that CDKE1 is a central nuclear component integrating mitochondrial and plastid retrograde signals and plays a role in regulating energy metabolism during the response to stress.},
language = {en},
number = {1640},
urldate = {2021-06-08},
journal = {Philosophical Transactions of the Royal Society B: Biological Sciences},
author = {Blanco, Nicolás E. and Guinea-Díaz, Manuel and Whelan, James and Strand, Åsa},
month = apr,
year = {2014},
pages = {20130231},
}
Downloads: 1
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Genetic defects in mitochondrial function result in an excessive reduction and energization of the chloroplast. Thus, it is clear that the activities of mitochondria and plastids need to be coordinated, but the manner by which the organelles communicate to coordinate their activities is unknown. The regulator of alternative oxidase ( rao1) mutant was isolated as a mutant unable to induce AOX1a expression in response to the inhibitor of the mitochondrial cytochrome c reductase (complex III), antimycin A. RAO1 encodes the nuclear localized cyclin-dependent kinase E1 (CDKE1). Interestingly, the rao1 mutant demonstrates a genome uncoupled phenotype also in response to redox changes in the photosynthetic electron transport chain. Thus, CDKE1 was shown to regulate both LIGHT HARVESTING COMPLEX B ( LHCB ) and ALTERNATIVE OXIDASE 1 ( AOX1a ) expression in response to retrograde signals. 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In addition, mitochondrial respiration protects photosynthesis against photoinhibition by dissipating excess redox equivalents from the chloroplasts. Genetic defects in mitochondrial function result in an excessive reduction and energization of the chloroplast. Thus, it is clear that the activities of mitochondria and plastids need to be coordinated, but the manner by which the organelles communicate to coordinate their activities is unknown. The\n regulator of alternative oxidase\n (\n rao1)\n mutant was isolated as a mutant unable to induce\n AOX1a\n expression in response to the inhibitor of the mitochondrial cytochrome\n c\n reductase (complex III), antimycin A.\n RAO1\n encodes the nuclear localized cyclin-dependent kinase E1 (CDKE1). Interestingly, the\n rao1\n mutant demonstrates a genome uncoupled phenotype also in response to redox changes in the photosynthetic electron transport chain. 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