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Riccardo Maraspini, Chen-Ho Wang, Alf Honigmann
Optimization of 2D and 3D cell culture to study membrane organization with STED microscopy
J Phys D: Appl Phys, 53(1) Art. No. 014001 (2020)
Source

Epithelia cells assemble into sheets that compartmentalize organs and generate tissue barriers. This is achieved by forming polarized membrane domains, which are connected by junctional complexes. While much is known about the organization of the basal membrane due to its easy accessibility by high and super-resolution microscopy, the apical and lateral membrane domains remain poorly characterized. Here we describe our methods to study the molecular organization of apical and lateral membrane domains by combining 2D and 3D epithelial cell culture with super-resolution STED microscopy. We show that inverted cell monolayers enable live cell imaging of the apical membrane with a resolution sufficient to resolve the densely packed micro-villi of human enterocytes. Furthermore, 3D cell culture enables us to resolve adhesion complexes in the lateral domain of kidney derived cells. We envision that these methods will help to reveal the supra-molecular structure of lateral and apical membrane domains in epithelial cells.

@article{Maraspini7567,
author={Riccardo Maraspini, Chen-Ho Wang, Alf Honigmann},
title={Optimization of 2D and 3D cell culture to study membrane organization with STED microscopy},
journal ={Journal of Physics D: Applied Physics},
volume={53},
issue ={1},
pages={1--1},
year=2020
}

Sean P A Ritter, Allison Lewis, Shelby L Vincent, Li Ling Lo, Ana Margarida da Conceicao Cunha, Danuta Chamot, Ingo Ensminger, George S Espie, George W Owttrim
Evidence for convergent sensing of multiple abiotic stresses in cyanobacteria.
Biochim Biophys Acta Gen Subj, 1864(1) Art. No. 129462 (2020)
PubMed Source

Bacteria routinely utilize two-component signal transduction pathways to sense and alter gene expression in response to environmental cues. While cyanobacteria express numerous two-component systems, these pathways do not regulate all of the genes within many of the identified abiotic stress-induced regulons.

@article{Ritter7572,
author={Sean P A Ritter, Allison Lewis, Shelby L Vincent, Li Ling Lo, Ana Margarida da Conceicao Cunha, Danuta Chamot, Ingo Ensminger, George S Espie, George W Owttrim},
title={Evidence for convergent sensing of multiple abiotic stresses in cyanobacteria.},
journal ={Biochimica et biophysica acta. General subjects},
volume={1864},
issue ={1},
pages={null--null},
year=2020
}

Virag Sharma, Michael Hiller
Losses of human disease-associated genes in placental mammals
NAR Genomics and Bioinformatics, 2(1) Art. No. doi: 10.1093/nargab/lqz012 (2020)
Source

@article{Sharma7569,
author={Virag Sharma, Michael Hiller},
title={Losses of human disease-associated genes in placental mammals},
journal ={NAR Genomics and Bioinformatics},
volume={2},
issue ={1},
pages={1--1},
year=2020
}

Yuting Wang, Sebastian Hinz, Ortrud Uckermann, Pia Hönscheid, Witigo von Schönfels, Greta Burmeister, Alexander Hendricks, Jacobo Miranda Ackerman, Gustavo Baretton, Jochen Hampe, Mario Brosch, Clemens Schafmayer, Andrej Shevchenko, Sebastian Zeissig
Shotgun lipidomics-based characterization of the landscape of lipid metabolism in colorectal cancer.
Biochim Biophys Acta Mol Cell Biol Lipids, 1865(3) Art. No. 158579 (2020)
PubMed Source

Solid tumors are characterized by global metabolic alterations which contribute to their growth and progression. Altered gene expression profiles and plasma lipid composition suggested a role for metabolic reprogramming in colorectal cancer (CRC) development. However, a conclusive picture of CRC-associated lipidome alterations in the tumor tissue has not emerged. Here, we determined molar abundances of 342 species from 20 lipid classes in matched biopsies of CRC and adjacent normal mucosa. We demonstrate that in contrast to previous reports, CRC shows a largely preserved lipidome composition that resembles that of normal colonic mucosa. Important exceptions include increased levels of lyso-phosphatidylinositols in CRC and reduced abundance of ether phospholipids in advanced stages of CRC. As such, our observations challenge the concept of widespread alterations in lipid metabolism in CRC and rather suggest changes in the cellular lipid profile that are limited to selected lipids involved in signaling and the scavenging of reactive oxygen species.

@article{Wang7575,
author={Yuting Wang, Sebastian Hinz, Ortrud Uckermann, Pia Hönscheid, Witigo von Schönfels, Greta Burmeister, Alexander Hendricks, Jacobo Miranda Ackerman, Gustavo Baretton, Jochen Hampe, Mario Brosch, Clemens Schafmayer, Andrej Shevchenko, Sebastian Zeissig},
title={Shotgun lipidomics-based characterization of the landscape of lipid metabolism in colorectal cancer.},
journal ={Biochimica et biophysica acta. Molecular and cell biology of lipids},
volume={1865},
issue ={3},
pages={null--null},
year=2020
}

Paulo Caldas, Mar López-Pelegrín, Daniel J G Pearce, Nazmi Burak Budanur, Jan Brugués, Martin Loose
Cooperative ordering of treadmilling filaments in cytoskeletal networks of FtsZ and its crosslinker ZapA.
Nat Commun, 10(1) Art. No. 5744 (2019)
PubMed Source

During bacterial cell division, the tubulin-homolog FtsZ forms a ring-like structure at the center of the cell. This Z-ring not only organizes the division machinery, but treadmilling of FtsZ filaments was also found to play a key role in distributing proteins at the division site. What regulates the architecture, dynamics and stability of the Z-ring is currently unknown, but FtsZ-associated proteins are known to play an important role. Here, using an in vitro reconstitution approach, we studied how the well-conserved protein ZapA affects FtsZ treadmilling and filament organization into large-scale patterns. Using high-resolution fluorescence microscopy and quantitative image analysis, we found that ZapA cooperatively increases the spatial order of the filament network, but binds only transiently to FtsZ filaments and has no effect on filament length and treadmilling velocity. Together, our data provides a model for how FtsZ-associated proteins can increase the precision and stability of the bacterial cell division machinery in a switch-like manner.

@article{Caldas7573,
author={Paulo Caldas, Mar López-Pelegrín, Daniel J G Pearce, Nazmi Burak Budanur, Jan Brugués, Martin Loose},
title={Cooperative ordering of treadmilling filaments in cytoskeletal networks of FtsZ and its crosslinker ZapA.},
journal ={Nature communications},
volume={10},
issue ={1},
pages={null--null},
year=2019
}

Gopi Shah, Konstantin Thierbach, Benjamin Schmid, Jens Waschke, Anna Reade, Mario Hlawitschka, Ingo Roeder, Nico Scherf, Jan Huisken
Multi-scale imaging and analysis identify pan-embryo cell dynamics of germlayer formation in zebrafish.
Nat Commun, 10(1) Art. No. 5753 (2019)
PubMed Source

The coordination of cell movements across spatio-temporal scales ensures precise positioning of organs during vertebrate gastrulation. Mechanisms governing such morphogenetic movements have been studied only within a local region, a single germlayer or in whole embryos without cell identity. Scale-bridging imaging and automated analysis of cell dynamics are needed for a deeper understanding of tissue formation during gastrulation. Here, we report pan-embryo analyses of formation and dynamics of all three germlayers simultaneously within a developing zebrafish embryo. We show that a distinct distribution of cells in each germlayer is established during early gastrulation via cell movement characteristics that are predominantly determined by their position in the embryo. The differences in initial germlayer distributions are subsequently amplified by a global movement, which organizes the organ precursors along the embryonic body axis, giving rise to the blueprint of organ formation. The tools and data are available as a resource for the community.

@article{Shah7574,
author={Gopi Shah, Konstantin Thierbach, Benjamin Schmid, Jens Waschke, Anna Reade, Mario Hlawitschka, Ingo Roeder, Nico Scherf, Jan Huisken},
title={Multi-scale imaging and analysis identify pan-embryo cell dynamics of germlayer formation in zebrafish.},
journal ={Nature communications},
volume={10},
issue ={1},
pages={null--null},
year=2019
}

Gema Gómez-Mariano, Nerea Matamala, Selene Martínez, Iago Justo, Alberto Marcacuzco, Carlos Jimenez, Sara Monzón, Isabel Cuesta, Cristina Garfia, María Teresa Martínez, Meritxell Huch, Ignacio Pérez de Castro, Manuel Posada, Sabina Janciauskiene, Beatriz Martínez-Delgado
Liver organoids reproduce alpha-1 antitrypsin deficiency-related liver disease.
Hepatol Int, Art. No. doi: 10.1007/s12072-019-10007-y (2019)
PubMed Source

Alpha-1 antitrypsin (AAT) is a product of SERPINA1 gene mainly expressed by hepatocytes. Clinically relevant mutations in the SERPINA1 gene, such as Z (Glu342Lys), results in an expression of misfolded AAT protein having high propensity to polymerize, accumulate in hepatocytes and thus to enhance a risk for hepatocyte damage and subsequent liver disease. So far, the relationship between the Z-AAT accumulation and liver cell damage remains not completely understood. We present three-dimensional organoid culture systems, as a novel tool for modeling Z-AAT-related liver diseases.

@article{Gómez-Mariano7582,
author={Gema Gómez-Mariano, Nerea Matamala, Selene Martínez, Iago Justo, Alberto Marcacuzco, Carlos Jimenez, Sara Monzón, Isabel Cuesta, Cristina Garfia, María Teresa Martínez, Meritxell Huch, Ignacio Pérez de Castro, Manuel Posada, Sabina Janciauskiene, Beatriz Martínez-Delgado},
title={Liver organoids reproduce alpha-1 antitrypsin deficiency-related liver disease.},
journal ={Hepatology international},
volume={},
pages={1--1},
year=2019
}

Takashi Namba, Judit Dóczi, Anneline Pinson, Lei Xing, Nereo Kalebic, Michaela Wilsch-Bräuninger, Katherine S. Long, Samir Vaid, Janelle Lauer, Aliona Bogdanova, Barbara Borgonovo, Anna Shevchenko, Patrick Keller, David N. Drechsel, Teymuras V. Kurzchalia, Pauline Wimberger, Christos Chinopoulos, Wieland Huttner
Human-Specific ARHGAP11B Acts in Mitochondria to Expand Neocortical Progenitors by Glutaminolysis.
Neuron, Art. No. doi: 10.1016/j.neuron.2019.11.027 (2019)
PubMed Source

The human-specific gene ARHGAP11B is preferentially expressed in neural progenitors of fetal human neocortex and increases abundance and proliferation of basal progenitors (BPs), which have a key role in neocortex expansion. ARHGAP11B has therefore been implicated in the evolutionary expansion of the human neocortex, but its mode of action has been unknown. Here, we show that ARHGAP11B is imported into mitochondria, where it interacts with the adenine nucleotide translocase (ANT) and inhibits the mitochondrial permeability transition pore (mPTP). BP expansion by ARHGAP11B requires its presence in mitochondria, and pharmacological inhibition of ANT function or mPTP opening mimic BP expansion by ARHGAP11B. Searching for the underlying metabolic basis, we find that BP expansion by ARHGAP11B requires glutaminolysis, the conversion of glutamine to glutamate for the tricarboxylic acid (TCA) cycle. Hence, an ARHGAP11B-induced, mitochondria-based effect on BP metabolism that is a hallmark of highly mitotically active cells appears to underlie its role in neocortex expansion.

@article{Namba7585,
author={Takashi Namba, Judit Dóczi, Anneline Pinson, Lei Xing, Nereo Kalebic, Michaela Wilsch-Bräuninger, Katherine S. Long, Samir Vaid, Janelle Lauer, Aliona Bogdanova, Barbara Borgonovo, Anna Shevchenko, Patrick Keller, David N. Drechsel, Teymuras V. Kurzchalia, Pauline Wimberger, Christos Chinopoulos, Wieland Huttner},
title={Human-Specific ARHGAP11B Acts in Mitochondria to Expand Neocortical Progenitors by Glutaminolysis.},
journal ={Neuron},
volume={},
pages={1--1},
year=2019
}

Kaushikaram Subramanian, Martin Weigert, Oliver Borsch, Heike Petzold, Alfonso Garcia-Ulloa, Eugene W Myers, Marius Ader, Irina Solovei, Moritz Kreysing
Rod nuclear architecture determines contrast transmission of the retina and behavioral sensitivity in mice.
Elife, 8 Art. No. e49542 (2019)
PubMed Source

Rod photoreceptors of nocturnal mammals display a striking inversion of nuclear architecture, which has been proposed as an evolutionary adaptation to dark environments. However, the nature of visual benefits and the underlying mechanisms remains unclear. It is widely assumed that improvements in nocturnal vision would depend on maximization of photon capture at the expense of image detail. Here we show that retinal optical quality improves 2-fold during terminal development, and that this enhancement is caused by nuclear inversion. We further demonstrate that improved retinal contrast transmission, rather than photon-budget or resolution, enhances scotopic contrast sensitivity by 18-27%, and improves motion detection capabilities up to 10-fold in dim environments. Our findings therefore add functional significance to a prominent exception of nuclear organization and establish retinal contrast transmission as a decisive determinant of mammalian visual perception.

@article{Subramanian7586,
author={Kaushikaram Subramanian, Martin Weigert, Oliver Borsch, Heike Petzold, Alfonso Garcia-Ulloa, Eugene W Myers, Marius Ader, Irina Solovei, Moritz Kreysing},
title={Rod nuclear architecture determines contrast transmission of the retina and behavioral sensitivity in mice.},
journal ={eLife},
volume={8},
pages={1--1},
year=2019
}

Matthäus Mittasch, Vanna M. Tran, Manolo U. Rios, Anatol W Fritsch, Stephen Enos, Beatriz Ferreira Gomes, Alec Bond, Moritz Kreysing, Jeffrey Woodruff
Material aging causes centrosome weakening and disassembly during mitotic exit
bioRxiv, Art. No. 866434 (2019)
Source

Centrosomes must resist microtubule-mediated forces for mitotic chromosome segregation. During mitotic exit, however, centrosomes are deformed and fractured by those same forces, which is a key step in centrosome disassembly. How the functional material properties of centrosomes change throughout the cell cycle, and how they are molecularly tuned remain unknown. Here, we used optically-induced flow perturbations to determine the molecular basis of centrosome strength and ductility in C. elegans embryos. We found that both properties declined sharply at anaphase onset, long before natural disassembly. This mechanical transition required PP2A phosphatase and correlated with inactivation of PLK-1 (Polo Kinase) and SPD-2 (Cep192). In vitro, PLK-1 and SPD-2 directly protected centrosome scaffolds from force-induced disassembly. Our results suggest that, prior to anaphase, PLK-1 and SPD-2 confer strength and ductility to the centrosome scaffold so that it can resist microtubule-pulling forces. In anaphase, centrosomes lose PLK-1 and SPD-2 and transition to a weak, brittle state that enables force-mediated centrosome disassembly.

@article{Mittasch7566,
author={Matthäus Mittasch, Vanna M. Tran, Manolo U. Rios, Anatol W Fritsch, Stephen Enos, Beatriz Ferreira Gomes, Alec Bond, Moritz Kreysing, Jeffrey Woodruff},
title={Material aging causes centrosome weakening and disassembly during mitotic exit},
journal ={bioRxiv},
volume={},
pages={1--1},
year=2019
}