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Article ; Online: How to analyze mitochondrial morphology in healthy cells and apoptotic cells in Caenorhabditis elegans.

Rolland, Stéphane G

2014 Volume 544, Page(s) 75–98

Abstract: Mitochondria constantly undergo fusion and fission events. A proper balance of fusion and fission is essential in healthy cells, as disrupting this balance is associated with several neurodegenerative diseases. Mitochondrial fission has also been shown ... ...

Abstract	Mitochondria constantly undergo fusion and fission events. A proper balance of fusion and fission is essential in healthy cells, as disrupting this balance is associated with several neurodegenerative diseases. Mitochondrial fission has also been shown to play an important role during apoptosis. Hence, the machineries that control mitochondrial morphology have both nonapoptotic and apoptotic functions. Seminal work in yeast has identified some of the key components of these machineries. However, the list is certainly not complete and new factors that are specific to metazoans are being identified every year. In this review, we describe methodologies to test whether a particular candidate gene plays a role in the control of mitochondrial morphology in healthy cells and apoptotic cells using Caenorhabditis elegans.
MeSH term(s)	Animals ; Apoptosis ; Caenorhabditis elegans/cytology ; Caenorhabditis elegans/embryology ; Caenorhabditis elegans/genetics ; Coloring Agents/analysis ; Equipment Design ; Gene Expression Regulation ; Luminescent Proteins/analysis ; Luminescent Proteins/genetics ; Microscopy, Fluorescence/instrumentation ; Microscopy, Fluorescence/methods ; Mitochondria/genetics ; Mitochondria/ultrastructure
Chemical Substances	Coloring Agents ; Luminescent Proteins
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	1557-7988 ; 0076-6879
ISSN (online)	1557-7988
ISSN	0076-6879
DOI	10.1016/B978-0-12-417158-9.00004-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: New Imaging Tools to Analyze Mitochondrial Morphology in Caenorhabditis elegans.

Regmi, Saroj G / Rolland, Stéphane G

Methods in molecular biology (Clifton, N.J.)

2017 Volume 1567, Page(s) 255–272

Abstract: Mitochondria are highly dynamic organelles that constantly fuse and divide. This process is essential as several neurodegenerative diseases have been associated with defects in mitochondrial fusion or fission. Several tools have been developed over the ... ...

Abstract	Mitochondria are highly dynamic organelles that constantly fuse and divide. This process is essential as several neurodegenerative diseases have been associated with defects in mitochondrial fusion or fission. Several tools have been developed over the years to visualize mitochondria in organisms such as Caenorhabditis elegans. Combining these tools with the powerful genetics of C. elegans has led to the discovery of new regulators of mitochondrial morphology. In this chapter, we present additional tools to further characterize mitochondrial morphology as well as regulators of mitochondrial morphology. Specifically, we introduce a photoactivatable mitoGFP (PAmitoGFP) that allows to investigate the connectivity of complex mitochondrial networks. In addition, we describe an immunostaining protocol that enables localization studies of these newly identified regulators of mitochondrial morphology.
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-6824-4_16
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Article ; Online: Genome-wide RNAi screen for regulators of UPRmt in Caenorhabditis elegans mutants with defects in mitochondrial fusion.

Haeussler, Simon / Yeroslaviz, Assa / Rolland, Stéphane G / Luehr, Sebastian / Lambie, Eric J / Conradt, Barbara

G3 (Bethesda, Md.)

2021 Volume 11, Issue 7

Abstract: Mitochondrial dynamics plays an important role in mitochondrial quality control and the adaptation of metabolic activity in response to environmental changes. The disruption of mitochondrial dynamics has detrimental consequences for mitochondrial and ... ...

Abstract	Mitochondrial dynamics plays an important role in mitochondrial quality control and the adaptation of metabolic activity in response to environmental changes. The disruption of mitochondrial dynamics has detrimental consequences for mitochondrial and cellular homeostasis and leads to the activation of the mitochondrial unfolded protein response (UPRmt), a quality control mechanism that adjusts cellular metabolism and restores homeostasis. To identify genes involved in the induction of UPRmt in response to a block in mitochondrial fusion, we performed a genome-wide RNAi screen in Caenorhabditis elegans mutants lacking the gene fzo-1, which encodes the ortholog of mammalian Mitofusin, and identified 299 suppressors and 86 enhancers. Approximately 90% of these 385 genes are conserved in humans, and one-third of the conserved genes have been implicated in human disease. Furthermore, many have roles in developmental processes, which suggests that mitochondrial function and their response to stress are defined during development and maintained throughout life. Our dataset primarily contains mitochondrial enhancers and non-mitochondrial suppressors of UPRmt, indicating that the maintenance of mitochondrial homeostasis has evolved as a critical cellular function, which, when disrupted, can be compensated for by many different cellular processes. Analysis of the subsets "non-mitochondrial enhancers" and "mitochondrial suppressors" suggests that organellar contact sites, especially between the ER and mitochondria, are of importance for mitochondrial homeostasis. In addition, we identified several genes involved in IP3 signaling that modulate UPRmt in fzo-1 mutants and found a potential link between pre-mRNA splicing and UPRmt activation.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Mitochondrial Dynamics/genetics ; RNA Interference ; Unfolded Protein Response/genetics
Chemical Substances	Caenorhabditis elegans Proteins ; FZO-1 protein, C elegans (EC 3.6.1.-) ; GTP Phosphohydrolases (EC 3.6.1.-)
Language	English
Publishing date	2021-04-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2629978-1
ISSN	2160-1836 ; 2160-1836
ISSN (online)	2160-1836
ISSN	2160-1836
DOI	10.1093/g3journal/jkab095
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Article ; Online: The histone chaperone SPT2 regulates chromatin structure and function in Metazoa.

Nature structural & molecular biology

2024 Volume 31, Issue 3, Page(s) 523–535

Abstract: Histone chaperones control nucleosome density and chromatin structure. In yeast, the H3-H4 chaperone Spt2 controls histone deposition at active genes but its roles in metazoan chromatin structure and organismal physiology are not known. Here we identify ... ...

Abstract	Histone chaperones control nucleosome density and chromatin structure. In yeast, the H3-H4 chaperone Spt2 controls histone deposition at active genes but its roles in metazoan chromatin structure and organismal physiology are not known. Here we identify the Caenorhabditis elegans ortholog of SPT2 (CeSPT-2) and show that its ability to bind histones H3-H4 is important for germline development and transgenerational epigenetic gene silencing, and that spt-2 null mutants display signatures of a global stress response. Genome-wide profiling showed that CeSPT-2 binds to a range of highly expressed genes, and we find that spt-2 mutants have increased chromatin accessibility at a subset of these loci. We also show that SPT2 influences chromatin structure and controls the levels of soluble and chromatin-bound H3.3 in human cells. Our work reveals roles for SPT2 in controlling chromatin structure and function in Metazoa.
MeSH term(s)	Animals ; Humans ; Histone Chaperones/genetics ; Histone Chaperones/metabolism ; DNA-Binding Proteins/metabolism ; Histones/metabolism ; Chromatin/metabolism ; Nucleosomes/metabolism ; Saccharomyces cerevisiae/metabolism
Chemical Substances	Histone Chaperones ; DNA-Binding Proteins ; Histones ; Chromatin ; Nucleosomes
Language	English
Publishing date	2024-01-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2126708-X
ISSN	1545-9985 ; 1545-9993
ISSN (online)	1545-9985
ISSN	1545-9993
DOI	10.1038/s41594-023-01204-3
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Article ; Online: Factors predictive of adherence to a non-pharmacological intervention in nursing home research: a substudy of the LEDEN trial

Chrusciel, Jan / Letty, Aude / Armaingaud, Didier / Barreto, Philippe / Berrut, Gilles / Rolland, Yves / Sanchez, Stéphane

Geriatrie et psychologie neuropsychiatrie du vieillissement

2022 Volume 20, Issue 2, Page(s) 199–207

Abstract: Introduction: Few older people participate in medical research, especially in the nursing home setting. The lack of evidence in this population may limit our ability to provide evidence-based treatments. This can partly be explained by difficulties in ... ...

Title translation	Facteurs associés à l’observance d’une intervention non médicamenteuse au cours d’une recherche menée en Établissement d’hébergement pour personnes âgées dépendantes (Ehpad) : une analyse secondaire de l’étude LEDEN
Abstract	Introduction: Few older people participate in medical research, especially in the nursing home setting. The lack of evidence in this population may limit our ability to provide evidence-based treatments. This can partly be explained by difficulties in obtaining a satisfactory adherence to research in this population, especially when the practice of a physical activity is needed. In this study data from the LEDEN trial (Effects of a Long-term Exercise Program on Functional Ability in People with Dementia Living in Nursing Homes: A Cluster Randomized Controlled Trial) was used to determine the predictors of adherence to the study protocol. Methods: Retrospective cohort study based on the data from the cluster randomized, controlled LEDEN trial. The LEDEN trial aimed to compare the effects of an exercise intervention with a nonphysical intervention on the ability to perform activities of daily living. Predictors of adherence (being present at ≥ 75% of sessions of the LEDEN trial) were identified by multivariable logistic regression. Results: By univariate analysis, the EVIBE scale (EValuation Immédiate du Bien-Être – evaluation of instantaneous well-being) measured at baseline was associated with study adherence, whereby higher scores were associated with higher adherence: 16.7% (1/6), 44.4% (4/9), 56.5% (13/23), 48.1% (13/27) and 75.0% (15/20) respectively for EVIBE scores from 1 to 5 (P = 0.02 for trend). By multi-variable analysis, an EVIBE scale score ≥ 4 did not predict clinical trial adherence (odds ratio [OR] 1.554, 95% confidence interval [CI] 0.619–3.942). Adherence was found to be lower among persons aged ≥ 95 years (OR: 0.121, 95%CI: 0.006–0.982). Conclusion: Older age (≥ 95 years) was associated with lower adherence to the study protocol. Further studies are needed to better understand and anticipate obstacles to adherence in research, while respecting consent procedures and patient autonomy.
MeSH term(s)	Activities of Daily Living ; Aged ; Exercise ; Humans ; Nursing Homes ; Retrospective Studies ; Skilled Nursing Facilities
Language	French
Publishing date	2022-08-05
Publishing country	France
Document type	Journal Article ; Randomized Controlled Trial
ISSN	2115-7863
ISSN (online)	2115-7863
DOI	10.1684/pnv.2022.1037
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Article ; Online: MitoSegNet: Easy-to-use Deep Learning Segmentation for Analyzing Mitochondrial Morphology.

Fischer, Christian A / Besora-Casals, Laura / Rolland, Stéphane G / Haeussler, Simon / Singh, Kritarth / Duchen, Michael / Conradt, Barbara / Marr, Carsten

iScience

2020 Volume 23, Issue 10, Page(s) 101601

Abstract: While the analysis of mitochondrial morphology has emerged as a key tool in the study of mitochondrial function, efficient quantification of mitochondrial microscopy images presents a challenging task and bottleneck for statistically robust conclusions. ... ...

Abstract	While the analysis of mitochondrial morphology has emerged as a key tool in the study of mitochondrial function, efficient quantification of mitochondrial microscopy images presents a challenging task and bottleneck for statistically robust conclusions. Here, we present Mitochondrial Segmentation Network (MitoSegNet), a pretrained deep learning segmentation model that enables researchers to easily exploit the power of deep learning for the quantification of mitochondrial morphology. We tested the performance of MitoSegNet against three feature-based segmentation algorithms and the machine-learning segmentation tool Ilastik. MitoSegNet outperformed all other methods in both pixelwise and morphological segmentation accuracy. We successfully applied MitoSegNet to unseen fluorescence microscopy images of mitoGFP expressing mitochondria in wild-type and
Language	English
Publishing date	2020-09-29
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2020.101601
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Article ; Online: MitoSegNet

Christian A. Fischer / Laura Besora-Casals / Stéphane G. Rolland / Simon Haeussler / Kritarth Singh / Michael Duchen / Barbara Conradt / Carsten Marr

iScience, Vol 23, Iss 10, Pp 101601- (2020)

Easy-to-use Deep Learning Segmentation for Analyzing Mitochondrial Morphology

2020

Abstract: Summary: While the analysis of mitochondrial morphology has emerged as a key tool in the study of mitochondrial function, efficient quantification of mitochondrial microscopy images presents a challenging task and bottleneck for statistically robust ... ...

Abstract	Summary: While the analysis of mitochondrial morphology has emerged as a key tool in the study of mitochondrial function, efficient quantification of mitochondrial microscopy images presents a challenging task and bottleneck for statistically robust conclusions. Here, we present Mitochondrial Segmentation Network (MitoSegNet), a pretrained deep learning segmentation model that enables researchers to easily exploit the power of deep learning for the quantification of mitochondrial morphology. We tested the performance of MitoSegNet against three feature-based segmentation algorithms and the machine-learning segmentation tool Ilastik. MitoSegNet outperformed all other methods in both pixelwise and morphological segmentation accuracy. We successfully applied MitoSegNet to unseen fluorescence microscopy images of mitoGFP expressing mitochondria in wild-type and catp-6ATP13A2 mutant C. elegans adults. Additionally, MitoSegNet was capable of accurately segmenting mitochondria in HeLa cells treated with fragmentation inducing reagents. We provide MitoSegNet in a toolbox for Windows and Linux operating systems that combines segmentation with morphological analysis.
Keywords	Cell Biology ; Bioinformatics ; Automation in Bioinformatics ; Artificial Intelligence ; Science ; Q
Subject code	004
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Autophagy compensates for defects in mitochondrial dynamics.

Haeussler, Simon / Köhler, Fabian / Witting, Michael / Premm, Madeleine F / Rolland, Stéphane G / Fischer, Christian / Chauve, Laetitia / Casanueva, Olivia / Conradt, Barbara

PLoS genetics

2020 Volume 16, Issue 3, Page(s) e1008638

Abstract: Compromising mitochondrial fusion or fission disrupts cellular homeostasis; however, the underlying mechanism(s) are not fully understood. The loss of C. elegans fzo-1MFN results in mitochondrial fragmentation, decreased mitochondrial membrane potential ... ...

Abstract	Compromising mitochondrial fusion or fission disrupts cellular homeostasis; however, the underlying mechanism(s) are not fully understood. The loss of C. elegans fzo-1MFN results in mitochondrial fragmentation, decreased mitochondrial membrane potential and the induction of the mitochondrial unfolded protein response (UPRmt). We performed a genome-wide RNAi screen for genes that when knocked-down suppress fzo-1MFN(lf)-induced UPRmt. Of the 299 genes identified, 143 encode negative regulators of autophagy, many of which have previously not been implicated in this cellular quality control mechanism. We present evidence that increased autophagic flux suppresses fzo-1MFN(lf)-induced UPRmt by increasing mitochondrial membrane potential rather than restoring mitochondrial morphology. Furthermore, we demonstrate that increased autophagic flux also suppresses UPRmt induction in response to a block in mitochondrial fission, but not in response to the loss of spg-7AFG3L2, which encodes a mitochondrial metalloprotease. Finally, we found that blocking mitochondrial fusion or fission leads to increased levels of certain types of triacylglycerols and that this is at least partially reverted by the induction of autophagy. We propose that the breakdown of these triacylglycerols through autophagy leads to elevated metabolic activity, thereby increasing mitochondrial membrane potential and restoring mitochondrial and cellular homeostasis.
MeSH term(s)	Animals ; Autophagy/genetics ; Autophagy/physiology ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Gene Expression Regulation/genetics ; Homeostasis/genetics ; Membrane Potential, Mitochondrial/genetics ; Membrane Potential, Mitochondrial/physiology ; Mitochondria/genetics ; Mitochondrial Dynamics/genetics ; Mitochondrial Proteins/genetics ; RNA Interference ; Unfolded Protein Response/genetics ; Unfolded Protein Response/physiology
Chemical Substances	Caenorhabditis elegans Proteins ; Mitochondrial Proteins ; FZO-1 protein, C elegans (EC 3.6.1.-) ; GTP Phosphohydrolases (EC 3.6.1.-)
Language	English
Publishing date	2020-03-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1008638
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Age-dependent changes in mitochondrial morphology and volume are not predictors of lifespan.

Regmi, Saroj G / Rolland, Stéphane G / Conradt, Barbara

Aging

2014 Volume 6, Issue 2, Page(s) 118–130

Abstract: Mitochondrial dysfunction is a hallmark of skeletal muscle degeneration during aging. One mechanism through which mitochondrial dysfunction can be caused is through changes in mitochondrial morphology. To determine the role of mitochondrial morphology ... ...

Abstract	Mitochondrial dysfunction is a hallmark of skeletal muscle degeneration during aging. One mechanism through which mitochondrial dysfunction can be caused is through changes in mitochondrial morphology. To determine the role of mitochondrial morphology changes in age-dependent mitochondrial dysfunction, we studied mitochondrial morphology in body wall muscles of the nematodeC. elegans. We found that in this tissue, animals display a tubular mitochondrial network, which fragments with increasing age. This fragmentation is accompanied by a decrease in mitochondrial volume. Mitochondrial fragmentation and volume loss occur faster under conditions that shorten lifespan and occur slower under conditions that increase lifespan. However, neither mitochondrial morphology nor mitochondrial volume of five- and seven-day old wild-type animals can be used to predict individual lifespan. Our results indicate that while mitochondria in body wall muscles undergo age-dependent fragmentation and a loss in volume, these changes are not the cause of aging but rather a consequence of the aging process.
MeSH term(s)	Aging/pathology ; Animals ; Caenorhabditis elegans ; Mitochondria/pathology ; Muscle Cells/pathology ; Temperature
Language	English
Publishing date	2014-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.100639
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Article ; Online: Reduced peroxisomal import triggers peroxisomal retrograde signaling.

Rackles, Elisabeth / Witting, Michael / Forné, Ignasi / Zhang, Xing / Zacherl, Judith / Schrott, Simon / Fischer, Christian / Ewbank, Jonathan J / Osman, Christof / Imhof, Axel / Rolland, Stéphane G

Cell reports

2021 Volume 34, Issue 3, Page(s) 108653

Abstract: Maintaining organelle function in the face of stress is known to involve organelle-specific retrograde signaling. Using Caenorhabditis elegans, we present evidence of the existence of such retrograde signaling for peroxisomes, which we define as the ... ...

Abstract	Maintaining organelle function in the face of stress is known to involve organelle-specific retrograde signaling. Using Caenorhabditis elegans, we present evidence of the existence of such retrograde signaling for peroxisomes, which we define as the peroxisomal retrograde signaling (PRS). Specifically, we show that peroxisomal import stress caused by knockdown of the peroxisomal matrix import receptor prx-5/PEX5 triggers NHR-49/peroxisome proliferator activated receptor alpha (PPARα)- and MDT-15/MED15-dependent upregulation of the peroxisomal Lon protease lonp-2/LONP2 and the peroxisomal catalase ctl-2/CAT. Using proteomic and transcriptomic analyses, we show that proteins involved in peroxisomal lipid metabolism and immunity are also upregulated upon prx-5(RNAi). While the PRS can be triggered by perturbation of peroxisomal β-oxidation, we also observed hallmarks of PRS activation upon infection with Pseudomonas aeruginosa. We propose that the PRS, in addition to a role in lipid metabolism homeostasis, may act as a surveillance mechanism to protect against pathogens.
MeSH term(s)	Animals ; Caenorhabditis elegans ; Peroxisomes/metabolism ; Signal Transduction
Language	English
Publishing date	2021-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.108653
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