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Frida W Lindberg, Till Korten, Anette Löfstrand, Mohammad A Rahman, Mariusz Graczyk, Alf Mansson, Heiner Linke, Ivan Maximov
Design and development of nanoimprint-enabled structures for molecular motor devices
Mater. Res. Express, 6(2) Art. No. 025057 (2019)
 

@article{Lindberg7307,
author={Frida W Lindberg, Till Korten, Anette Löfstrand, Mohammad A Rahman, Mariusz Graczyk, Alf Mansson, Heiner Linke, Ivan Maximov},
title={Design and development of nanoimprint-enabled structures for molecular motor devices},
journal ={Materials Research Express},
volume={6},
issue ={2},
pages={null--null},
year=2019
}

Antje Janosch, Carolin Kaffka, Marc Bickle
Unbiased Phenotype Detection Using Negative Controls
SLAS Discov, Art. No. doi: 10.1177/2472555218818053 (2019)
Supplementary Website Source  

@article{Janosch7217,
author={Antje Janosch, Carolin Kaffka, Marc Bickle},
title={Unbiased Phenotype Detection Using Negative Controls},
journal ={SLAS Discovery},
volume={},
pages={1--1},
year=2019
}

Albert Thommen, Steffen Werner, Olga Frank, Jenny Philipp, Oskar Knittelfelder, Yihui Quek, Karim Fahmy, Andrej Shevchenko, Benjamin Friedrich, Frank Jülicher, Jochen Rink
Body size-dependent energy storage causes Kleiber's law scaling of the metabolic rate in planarians.
Elife, 8 Art. No. e38187 (2019)
PubMed Source   

Kleiber's law, or the 3/4 -power law scaling of the metabolic rate with body mass, is considered one of the few quantitative laws in biology, yet its physiological basis remains unknown. Here, we report Kleiber's law scaling in the planarian Schmidtea mediterranea. Its reversible and life history-independent changes in adult body mass over 3 orders of magnitude reveal that Kleiber's law does not emerge from the size-dependent decrease in cellular metabolic rate, but from a size-dependent increase in mass per cell. Through a combination of experiment and theoretical analysis of the organismal energy balance, we further show that the mass allometry is caused by body size dependent energy storage. Our results reveal the physiological origins of Kleiber's law in planarians and have general implications for understanding a fundamental scaling law in biology.
@article{Thommen7306,
author={Albert Thommen, Steffen Werner, Olga Frank, Jenny Philipp, Oskar Knittelfelder, Yihui Quek, Karim Fahmy, Andrej Shevchenko, Benjamin Friedrich, Frank Jülicher, Jochen Rink},
title={Body size-dependent energy storage causes Kleiber's law scaling of the metabolic rate in planarians.},
journal ={eLife},
volume={8},
pages={null--null},
year=2019
}

Alexander Mietke, Frank Jülicher, Ivo F. Sbalzarini
Self-organized shape dynamics of active surfaces.
Proc Natl Acad Sci U.S.A., 116(1) 29-34 (2019)
PubMed Source   

Mechanochemical processes in thin biological structures, such as the cellular cortex or epithelial sheets, play a key role during the morphogenesis of cells and tissues. In particular, they are responsible for the dynamical organization of active stresses that lead to flows and deformations of the material. Consequently, advective transport redistributes force-generating molecules and thereby contributes to a complex mechanochemical feedback loop. It has been shown in fixed geometries that this mechanism enables patterning, but the interplay of these processes with shape changes of the material remains to be explored. In this work, we study the fully self-organized shape dynamics using the theory of active fluids on deforming surfaces and develop a numerical approach to solve the corresponding force and torque balance equations. We describe the spontaneous generation of nontrivial surface shapes, shape oscillations, and directed surface flows that resemble peristaltic waves from self-organized, mechanochemical processes on the deforming surface. Our approach provides opportunities to explore the dynamics of self-organized active surfaces and can help to understand the role of shape as an integral element of the mechanochemical organization of morphogenetic processes.
@article{Mietke7278,
author={Alexander Mietke, Frank Jülicher, Ivo F. Sbalzarini},
title={Self-organized shape dynamics of active surfaces.},
journal ={Proceedings of the National Academy of Sciences of the United States of America},
volume={116},
issue ={1},
pages={29--34},
year=2019
}

Nikolai Hecker, Virag Sharma, Michael Hiller
Convergent gene losses illuminate metabolic and physiological changes in herbivores and carnivores
Proc Natl Acad Sci U.S.A., 1-1 (2019)
 

@article{Hecker7300,
author={Nikolai Hecker, Virag Sharma, Michael Hiller},
title={Convergent gene losses illuminate metabolic and physiological changes in herbivores and carnivores},
journal ={Proceedings of the National Academy of Sciences of the United States of America},
volume={},
pages={1--1},
year=2019
}

Malte Lehmann, Elisabeth Knust, Sarita Hebbar
Drosophila melanogaster: A Valuable Genetic Model Organism to Elucidate the Biology of Retinitis Pigmentosa.
Methods Mol Biol, 1834 221-249 (2019)
PubMed Source   

Retinitis pigmentosa (RP) is a complex inherited disease. It is associated with mutations in a wide variety of genes with many different functions. These mutations impact the integrity of rod photoreceptors and ultimately result in the progressive degeneration of rods and cone photoreceptors in the retina, leading to complete blindness. A hallmark of this disease is the variable degree to which symptoms are manifest in patients. This is indicative of the influence of the environment, and/or of the distinct genetic makeup of the individual.The fruit fly, Drosophila melanogaster, has effectively proven to be a great model system to better understand interconnected genetic networks. Unraveling genetic interactions and thereby different cellular processes is relatively easy because more than a century of research on flies has enabled the creation of sophisticated genetic tools to perturb gene function. A remarkable conservation of disease genes across evolution and the similarity of the general organization of the fly and vertebrate photoreceptor cell had prompted research on fly retinal degeneration. To date six fly models for RP, including RP4, RP11, RP12, RP14, RP25, and RP26, have been established, and have provided useful information on RP disease biology. In this chapter, an outline of approaches and experimental specifications are described to enable utilizing or developing new fly models of RP.
@article{Lehmann7271,
author={Malte Lehmann, Elisabeth Knust, Sarita Hebbar},
title={Drosophila melanogaster: A Valuable Genetic Model Organism to Elucidate the Biology of Retinitis Pigmentosa.},
journal ={Methods in molecular biology (Clifton, N.J.)},
volume={1834},
pages={221--249},
year=2019
}

Monalisa Mishra, Elisabeth Knust
Analysis of the Drosophila Compound Eye with Light and Electron Microscopy.
Methods Mol Biol, 1834 345-364 (2019)
PubMed Source   

The Drosophila compound eye is composed of about 750 units, called ommatidia, which are arranged in a highly regular pattern. Eye development proceeds in a stereotypical fashion, where epithelial cells of the eye imaginal discs are specified, recruited, and differentiated in a sequential order that leads to the highly precise structure of an adult eye. Even small perturbations, for example in signaling pathways that control proliferation, cell death, or differentiation, can impair the regular structure of the eye, which can be easily detected and analyzed. In addition, the Drosophila eye has proven to be an ideal model for studying the genetic control of neurodegeneration, since the eye is not essential for viability. Several human neurodegeneration diseases have been modeled in the fly, leading to a better understanding of the function/misfunction of the respective gene. In many cases, the genes involved and their functions are conserved between flies and human. More strikingly, when ectopically expressed in the fly eye some human genes, even those without a Drosophila counterpart, can induce neurodegeneration, detectable by aberrant phototaxis, impaired electrophysiology, or defects in eye morphology and retinal histology. These defects are often rather subtle alteration in shape, size, or arrangement of the cells, and can be easily scored at the ultrastructural level. This chapter aims to provide an overview regarding the analysis of the retina by light and electron microscopy.
@article{Mishra7270,
author={Monalisa Mishra, Elisabeth Knust},
title={Analysis of the Drosophila Compound Eye with Light and Electron Microscopy.},
journal ={Methods in molecular biology (Clifton, N.J.)},
volume={1834},
pages={345--364},
year=2019
}

Makoto Saito, Daniel Hess, Jan Eglinger, Anatol Fritsch, Moritz Kreysing, Brian Weinert, Chunaram Choudhary, Patrick Matthias
Acetylation of intrinsically disordered regions regulates phase separation.
Nat Chem Biol, 15(1) 51-61 (2019)
PubMed Source   

Liquid-liquid phase separation (LLPS) of proteins containing intrinsically disordered regions (IDRs) has been proposed as a mechanism underlying the formation of membrane-less organelles. Tight regulation of IDR behavior is essential to ensure that LLPS only takes place when necessary. Here, we report that IDR acetylation/deacetylation regulates LLPS and assembly of stress granules (SGs), membrane-less organelles forming in response to stress. Acetylome analysis revealed that the RNA helicase DDX3X, an important component of SGs, is a novel substrate of the deacetylase HDAC6. The N-terminal IDR of DDX3X (IDR1) can undergo LLPS in vitro, and its acetylation at multiple lysine residues impairs the formation of liquid droplets. We also demonstrated that enhanced LLPS propensity through deacetylation of DDX3X-IDR1 by HDAC6 is necessary for SG maturation, but not initiation. Our analysis provides a mechanistic framework to understand how acetylation and deacetylation of IDRs regulate LLPS spatiotemporally, and impact membrane-less organelle formation in vivo.
@article{Saito7280,
author={Makoto Saito, Daniel Hess, Jan Eglinger, Anatol Fritsch, Moritz Kreysing, Brian Weinert, Chunaram Choudhary, Patrick Matthias},
title={Acetylation of intrinsically disordered regions regulates phase separation.},
journal ={Nature chemical biology},
volume={15},
issue ={1},
pages={51--61},
year=2019
}

Kristina Thamm, Deimantė Šimaitė, Jana Karbanová, Vicente Bermúdez, Doreen Reichert, Anne Morgenstern, Martin Bornhäuser, Wieland Huttner, Michaela Wilsch-Bräuninger, Denis Corbeil
Prominin-1 (CD133) modulates the architecture and dynamics of microvilli.
Traffic, 20(1) 39-60 (2019)
PubMed Source   

Prominin-1 is a cell surface biomarker that allows the identification of stem and cancer stem cells from different organs. It is also expressed in several differentiated epithelial and non-epithelial cells. Irrespective of the cell type, prominin-1 is associated with plasma membrane protrusions. Here, we investigate its impact on the architecture of membrane protrusions using microvilli of Madin-Darby canine kidney cells as the main model. Our high-resolution analysis revealed that upon the overexpression of prominin-1 the number of microvilli and clusters of them increased. Microvilli with branched and/or knob-like morphologies were observed and stimulated by mutations in the ganglioside-binding site of prominin-1. The altered phenotypes were caused by the interaction of prominin-1 with phosphoinositide 3-kinase and Arp2/3 complex. Mutation of tyrosine 828 of prominin-1 impaired its phosphorylation and thereby inhibited the aforementioned interactions abolishing altered microvilli. This suggests that the interplay of prominin-1-ganglioside membrane complexes, phosphoinositide 3-kinase and cytoskeleton components regulates microvillar architecture. Lastly, the expression of prominin-1 and its mutants modified the structure of filopodia emerging from fibroblast-like cells and silencing human prominin-1 in primary hematopoietic stem cells resulted in the loss of uropod-associated microvilli. Altogether, these findings strengthen the role of prominin-1 as an organizer of cellular protrusions.
@article{Thamm7266,
author={Kristina Thamm, Deimantė Šimaitė, Jana Karbanová, Vicente Bermúdez, Doreen Reichert, Anne Morgenstern, Martin Bornhäuser, Wieland Huttner, Michaela Wilsch-Bräuninger, Denis Corbeil},
title={Prominin-1 (CD133) modulates the architecture and dynamics of microvilli.},
journal ={Traffic (Copenhagen, Denmark)},
volume={20},
issue ={1},
pages={39--60},
year=2019
}

Corey A. H. Allard, Franziska Decker, Orion D. Weiner, Jared E. Toettcher, Brian R. Graziano
A size-invariant bud-duration timer enables robustness in yeast cell size control.
PLoS ONE, 13(12) Art. No. e0209301 (2018)
PubMed Source   

Cell populations across nearly all forms of life generally maintain a characteristic cell type-dependent size, but how size control is achieved has been a long-standing question. The G1/S boundary of the cell cycle serves as a major point of size control, and mechanisms operating here restrict passage of cells to Start if they are too small. In contrast, it is less clear how size is regulated post-Start, during S/G2/M. To gain further insight into post-Start size control, we prepared budding yeast that can be reversibly blocked from bud initiation. While blocked, cells continue to grow isotropically, increasing their volume by more than an order of magnitude over unperturbed cells. Upon release from their block, giant mothers reenter the cell cycle and their progeny rapidly return to the original unperturbed size. We found this behavior to be consistent with a size-invariant 'timer' specifying the duration of S/G2/M. These results indicate that yeast use at least two distinct mechanisms at different cell cycle phases to ensure size homeostasis.
@article{Allard7308,
author={Corey A. H. Allard, Franziska Decker, Orion D. Weiner, Jared E. Toettcher, Brian R. Graziano},
title={A size-invariant bud-duration timer enables robustness in yeast cell size control.},
journal ={PloS ONE},
volume={13},
issue ={12},
pages={null--null},
year=2018
}