@misc{KuekenSommerYanevaRoderetal.2018,
  author    = {K{\"u}ken, Anika and Sommer, Frederik and Yaneva-Roder, Liliya and Mackinder, Luke C.M. and H{\"o}hne, Melanie and Geimer, Stefan and Jonikas, Martin C. and Schroda, Michael and Stitt, Mark and Nikoloski, Zoran and Mettler-Altmann, Tabea},
  title     = {Effects of microcompartmentation on flux distribution and metabolic pools in Chlamydomonas reinhardtii chloroplasts},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {1122},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-44635},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-446358},
  pages     = {25},
  year      = {2018},
  abstract  = {Cells and organelles are not homogeneous but include microcompartments that alter the spatiotemporal characteristics of cellular processes. The effects of microcompartmentation on metabolic pathways are however difficult to study experimentally. The pyrenoid is a microcompartment that is essential for a carbon concentrating mechanism (CCM) that improves the photosynthetic performance of eukaryotic algae. Using Chlamydomonas reinhardtii, we obtained experimental data on photosynthesis, metabolites, and proteins in CCM-induced and CCM-suppressed cells. We then employed a computational strategy to estimate how fluxes through the Calvin-Benson cycle are compartmented between the pyrenoid and the stroma. Our model predicts that ribulose-1,5-bisphosphate (RuBP), the substrate of Rubisco, and 3-phosphoglycerate (3PGA), its product, diffuse in and out of the pyrenoid, respectively, with higher fluxes in CCM-induced cells. It also indicates that there is no major diffusional barrier to metabolic flux between the pyrenoid and stroma. Our computational approach represents a stepping stone to understanding microcompartmentalized CCM in other organisms.},
  language  = {en}
}
@article{KuekenSommerYanevaRoderetal.2018,
  author    = {K{\"u}ken, Anika and Sommer, Frederik and Yaneva-Roder, Liliya and Mackinder, Luke C. M. and Hoehne, Melanie and Geimer, Stefan and Jonikas, Martin C. and Schroda, Michael and Stitt, Mark and Nikoloski, Zoran and Mettler-Altmann, Tabea},
  title     = {Effects of microcompartmentation on flux distribution and metabolic pools in Chlamydomonas reinhardtii chloroplasts},
  series = {eLife},
  volume    = {7},
  journal   = {eLife},
  publisher = {eLife Sciences Publications},
  address   = {Cambridge},
  issn      = {2050-084X},
  doi       = {10.7554/eLife.37960},
  pages     = {23},
  year      = {2018},
  abstract  = {Cells and organelles are not homogeneous but include microcompartments that alter the spatiotemporal characteristics of cellular processes. The effects of microcompartmentation on metabolic pathways are however difficult to study experimentally. The pyrenoid is a microcompartment that is essential for a carbon concentrating mechanism (CCM) that improves the photosynthetic performance of eukaryotic algae. Using Chlamydomonas reinhardtii, we obtained experimental data on photosynthesis, metabolites, and proteins in CCM-induced and CCM-suppressed cells. We then employed a computational strategy to estimate how fluxes through the Calvin-Benson cycle are compartmented between the pyrenoid and the stroma. Our model predicts that ribulose-1,5-bisphosphate (RuBP), the substrate of Rubisco, and 3-phosphoglycerate (3PGA), its product, diffuse in and out of the pyrenoid, respectively, with higher fluxes in CCM-induced cells. It also indicates that there is no major diffusional barrier to metabolic flux between the pyrenoid and stroma. Our computational approach represents a stepping stone to understanding microcompartmentalized CCM in other organisms.},
  language  = {en}
}
@article{NordhuesSchoettlerUngeretal.2012,
  author    = {Nordhues, Andre and Sch{\"o}ttler, Mark Aurel and Unger, Ann-Katrin and Geimer, Stefan and Sch{\"o}nfelder, Stephanie and Schmollinger, Stefan and Ruetgers, Mark and Finazzi, Giovanni and Soppa, Barbara and Sommer, Frederik and M{\"u}hlhaus, Timo and Roach, Thomas and Krieger-Liszkay, Anja and Lokstein, Heiko and Luis Crespo, Jose and Schroda, Michael},
  title     = {Evidence for a role of VIPP1 in the structural organization of the photosynthetic apparatus in chlamydomonas},
  series = {The plant cell},
  volume    = {24},
  journal   = {The plant cell},
  number    = {2},
  publisher = {American Society of Plant Physiologists},
  address   = {Rockville},
  issn      = {1040-4651},
  doi       = {10.1105/tpc.111.092692},
  pages     = {637 -- 659},
  year      = {2012},
  abstract  = {The vesicle-inducing protein in plastids (VIPP1) was suggested to play a role in thylakoid membrane formation via membrane vesicles. As this functional assignment is under debate, we investigated the function of VIPP1 in Chlamydomonas reinhardtii. Using immunofluorescence, we localized VIPP1 to distinct spots within the chloroplast. In VIPP1-RNA interference/artificial microRNA cells, we consistently observed aberrant, prolamellar body-like structures at the origin of multiple thylakoid membrane layers, which appear to coincide with the immunofluorescent VIPP1 spots and suggest a defect in thylakoid membrane biogenesis. Accordingly, using quantitative shotgun proteomics, we found that unstressed vipp1 mutant cells accumulate 14 to 20\% less photosystems, cytochrome b(6)f complex, and ATP synthase but 30\% more light-harvesting complex II than control cells, while complex assembly, thylakoid membrane ultrastructure, and bulk lipid composition appeared unaltered. Photosystems in vipp1 mutants are sensitive to high light, which coincides with a lowered midpoint potential of the Q(A)/Q(A)(-) redox couple and increased thermosensitivity of photosystem II (PSII), suggesting structural defects in PSII. Moreover, swollen thylakoids, despite reduced membrane energization, in vipp1 mutants grown on ammonium suggest defects in the supermolecular organization of thylakoid membrane complexes. Overall, our data suggest a role of VIPP1 in the biogenesis/assembly of thylakoid membrane core complexes, most likely by supplying structural lipids.},
  language  = {en}
}
@article{HemmeVeyelMuehlhausetal.2014,
  author    = {Hemme, Dorothea and Veyel, Daniel and Muehlhaus, Timo and Sommer, Frederik and Jueppner, Jessica and Unger, Ann-Katrin and Sandmann, Michael and Fehrle, Ines and Schoenfelder, Stephanie and Steup, Martin and Geimer, Stefan and Kopka, Joachim and Giavalisco, Patrick and Schroda, Michael},
  title     = {Systems-wide analysis of acclimation responses to long-term heat stress and recovery in the photosynthetic model organism Chlamydomonas reinhardtii},
  series = {The plant cell},
  volume    = {26},
  journal   = {The plant cell},
  number    = {11},
  publisher = {American Society of Plant Physiologists},
  address   = {Rockville},
  issn      = {1040-4651},
  doi       = {10.1105/tpc.114.130997},
  pages     = {4270 -- 4297},
  year      = {2014},
  abstract  = {We applied a top-down systems biology approach to understand how Chlamydomonas reinhardtii acclimates to long-term heat stress (HS) and recovers from it. For this, we shifted cells from 25 to 42 degrees C for 24 h and back to 25 degrees C for >= 8 h and monitored abundances of 1856 proteins/protein groups, 99 polar and 185 lipophilic metabolites, and cytological and photosynthesis parameters. Our data indicate that acclimation of Chlamydomonas to long-term HS consists of a temporally ordered, orchestrated implementation of response elements at various system levels. These comprise (1) cell cycle arrest; (2) catabolism of larger molecules to generate compounds with roles in stress protection; (3) accumulation of molecular chaperones to restore protein homeostasis together with compatible solutes; (4) redirection of photosynthetic energy and reducing power from the Calvin cycle to the de novo synthesis of saturated fatty acids to replace polyunsaturated ones in membrane lipids, which are deposited in lipid bodies; and (5) when sinks for photosynthetic energy and reducing power are depleted, resumption of Calvin cycle activity associated with increased photorespiration, accumulation of reactive oxygen species scavengers, and throttling of linear electron flow by antenna uncoupling. During recovery from HS, cells appear to focus on processes allowing rapid resumption of growth rather than restoring pre-HS conditions.},
  language  = {en}
}