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Article ; Online: Neuronal miR-17-5p contributes to interhemispheric cortical connectivity defects induced by prenatal alcohol exposure.

Altounian, Mike / Bellon, Anaïs / Mann, Fanny

2023 Volume 42, Issue 9, Page(s) 113020

Abstract: Structural and functional deficits in brain connectivity are reported in patients with fetal alcohol spectrum disorders (FASDs), but whether and how prenatal alcohol exposure (PAE) affects axonal development of neurons and disrupts wiring between brain ... ...

Abstract	Structural and functional deficits in brain connectivity are reported in patients with fetal alcohol spectrum disorders (FASDs), but whether and how prenatal alcohol exposure (PAE) affects axonal development of neurons and disrupts wiring between brain regions is unknown. Here, we develop a mouse model of moderate alcohol exposure during prenatal brain wiring to study the effects of PAE on corpus callosum (CC) development. PAE induces aberrant navigation of interhemispheric CC axons that persists even after exposure ends, leading to ectopic termination in the contralateral cortex. The neuronal miR-17-5p and its target ephrin type A receptor 4 (EphA4) mediate the effect of alcohol on the contralateral targeting of CC axons. Thus, altered microRNA-mediated regulation of axonal guidance may have implications for interhemispheric cortical connectivity and associated behaviors in FASD.
Language	English
Publishing date	2023-08-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113020
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Article ; Online: Axon guidance molecules in liver pathology: Journeys on a damaged passport.

Chicherova, Ievgeniia / Hernandez, Charlotte / Mann, Fanny / Zoulim, Fabien / Parent, Romain

Liver international : official journal of the International Association for the Study of the Liver

2023 Volume 43, Issue 9, Page(s) 1850–1864

Abstract: Background and aims: The liver is an innervated organ that develops a variety of chronic liver disease (CLD). Axon guidance cues (AGCs), of which ephrins, netrins, semaphorins and slits are the main representative, are secreted or membrane-bound ... ...

Abstract	Background and aims: The liver is an innervated organ that develops a variety of chronic liver disease (CLD). Axon guidance cues (AGCs), of which ephrins, netrins, semaphorins and slits are the main representative, are secreted or membrane-bound proteins that can attract or repel axons through interactions with their growth cones that contain receptors recognizing these messengers. While fundamentally implicated in the physiological development of the nervous system, the expression of AGCs can also be reinduced under acute or chronic conditions, such as CLD, that necessitate redeployment of neural networks. Methods: This review considers the ad hoc literature through the neglected canonical neural function of these proteins that is also applicable to the diseased liver (and not solely their observed parenchymal impact). Results: AGCs impact fibrosis regulation, immune functions, viral/host interactions, angiogenesis, and cell growth, both at the CLD and HCC levels. Special attention has been paid to distinguishing correlative and causal data in such datasets in order to streamline data interpretation. While hepatic mechanistic insights are to date limited, bioinformatic evidence for the identification of AGCs mRNAs positive cells, protein expression, quantitative regulation, and prognostic data have been provided. Liver-pertinent clinical studies based on the US Clinical Trials database are listed. Future research directions derived from AGC targeting are proposed. Conclusion: This review highlights frequent implication of AGCs in CLD, linking traits of liver disorders and the local autonomic nervous system. Such data should contribute to diversifying current parameters of patient stratification and our understanding of CLD.
Language	English
Publishing date	2023-07-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2102783-3
ISSN	1478-3231 ; 1478-3223
ISSN (online)	1478-3231
ISSN	1478-3223
DOI	10.1111/liv.15662
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Zs.A 1632: Show issues

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Article ; Online: Tumorigenesis and axons regulation for the pancreatic cancer: A mathematical approach.

Chauvet, Sophie / Hubert, Florence / Mann, Fanny / Mezache, Mathieu

Journal of theoretical biology

2022 Volume 556, Page(s) 111301

Abstract: The nervous system is today recognized to play an important role in the development of cancer. Indeed, neurons extend long processes (axons) that grow and infiltrate tumors in order to regulate the progression of the disease in a positive or negative way, ...

Abstract	The nervous system is today recognized to play an important role in the development of cancer. Indeed, neurons extend long processes (axons) that grow and infiltrate tumors in order to regulate the progression of the disease in a positive or negative way, depending on the type of neuron considered. Mathematical modeling of this biological process allows to formalize the nerve-tumor interactions and to test hypotheses in silico to better understand this phenomenon. In this work, we introduce a system of differential equations modeling the progression of pancreatic ductal adenocarcinoma (PDAC) coupled with associated changes in axonal innervation. The study of the asymptotic behavior of the model confirms the experimental observations that PDAC development is correlated with the type and densities of axons in the tissue. We study then the identifiability and the sensitivity of the model parameters. The identifiability analysis informs on the adequacy between the parameters of the model and the experimental data and the sensitivity analysis on the most contributing factors on the development of cancer. It leads to significant insights on the main neural checkpoints and mechanisms controlling the progression of pancreatic cancer. Finally, we give an example of a simulation of the effects of partial or complete denervation that sheds lights on complex correlation between the healthy, pre-cancerous and cancerous cell densities and axons with opposite functions.
MeSH term(s)	Humans ; Pancreatic Neoplasms/pathology ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; Axons ; Cell Transformation, Neoplastic ; Carcinogenesis ; Gene Expression Regulation, Neoplastic ; Cell Line, Tumor ; Pancreatic Neoplasms
Language	English
Publishing date	2022-10-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2972-5
ISSN	1095-8541 ; 0022-5193
ISSN (online)	1095-8541
ISSN	0022-5193
DOI	10.1016/j.jtbi.2022.111301
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Zs.A 923: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Keeping up with advances in axon guidance.

Bellon, Anaïs / Mann, Fanny

Current opinion in neurobiology

2018 Volume 53, Page(s) 183–191

Abstract: Twenty-five years after the discovery of the first chemotropic molecules for growing axons, what are the new findings? This review describes the latest progress made in our understanding of the molecular control of axonal guidance in the vertebrate ... ...

Abstract	Twenty-five years after the discovery of the first chemotropic molecules for growing axons, what are the new findings? This review describes the latest progress made in our understanding of the molecular control of axonal guidance in the vertebrate nervous system. Special focus will be given to new molecular players, their source and location in vivo, and the role of membrane/receptor trafficking and RNA-based mechanisms in axon guidance cue signalling.
MeSH term(s)	Animals ; Axon Guidance/physiology ; Axons/metabolism ; Biological Transport/physiology ; Central Nervous System/growth & development ; Humans ; Nerve Net/growth & development
Language	English
Publishing date	2018-09-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1078046-4
ISSN	1873-6882 ; 0959-4388
ISSN (online)	1873-6882
ISSN	0959-4388
DOI	10.1016/j.conb.2018.09.004
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Zs.A 3260: Show issues

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Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Book ; Online: Tumorigenesis and axons regulation for the pancreatic cancer

Chauvet, Sophie / Hubert, Florence / Mann, Fanny / Mezache, Mathieu

a mathematical approach

2022

Abstract	The nervous system is today recognized to play an important role in the development of cancer. Indeed, neurons extend long processes (axons) that grow and infiltrate tumors in order to regulate the progression of the disease in a positive or negative way, depending on the type of neuron considered. Mathematical modelling of this biological process allows to formalize the nerve-tumor interactions and to test hypotheses in silico to better understand this phenomenon. In this work, we introduce a system of differential equations modelling the progression of pancreatic ductal adenocarcinoma (PDAC) coupled with associated changes in axonal innervation. The study of the asymptotic behavior of the model confirms the experimental observations that PDAC development is correlated with the type and densities of axons in the tissue. In addition, we study the identifiability of the model parameters. This informs on the adequacy between the parameters of the model and the experimental data. It leads to significant insights such that the transdifferentiation phenomenon accelerates during the development process of PDAC cells. Finally, we give an example of a simulation of the effects of partial or complete denervation that sheds lights on complex correlation between the cell populations and axons with opposite functions.
Keywords	Mathematics - Dynamical Systems ; Statistics - Applications
Subject code	612
Publishing date	2022-05-24
Publishing country	us
Document type	Book ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Characterizing Semaphorin Signaling Using Isolated Neurons in Culture.

Chauvet, Sophie / Mire, Erik / Mann, Fanny

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

2017 Volume 1493, Page(s) 223–235

Abstract: Semaphorin guidance molecules act through different receptor complexes to activate multiple signaling cascades leading to changes in axonal growth cone behavior and morphology. We describe here approaches for studying the effect of individual Semaphorins ...

Abstract	Semaphorin guidance molecules act through different receptor complexes to activate multiple signaling cascades leading to changes in axonal growth cone behavior and morphology. We describe here approaches for studying the effect of individual Semaphorins on isolated forebrain neurons from mouse embryos and dissecting downstream signaling pathways. These approaches include the production of recombinant Semaphorin ligands, the culture of dissociated primary neurons, the manipulation of gene expression by electroporation in primary neurons, and functional assays to assess axon outgrowth and growth cone collapse.
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-6448-2_16
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Article ; Online: The declaration of independence of the neurovascular intimacy.

Chauvet, Sophie / Mann, Fanny

Neuron

2013 Volume 80, Issue 2, Page(s) 262–265

Abstract: In this issue of Neuron, Oh and Gu (2013) present a model in which intimately related embryonic nerves and blood vessels are patterned independently in response to different guidance cues from a central organizer: the whisker. ...

Abstract	In this issue of Neuron, Oh and Gu (2013) present a model in which intimately related embryonic nerves and blood vessels are patterned independently in response to different guidance cues from a central organizer: the whisker.
MeSH term(s)	Animals ; Blood Vessels/physiology ; Body Patterning/physiology ; Sensory Receptor Cells/physiology ; Vibrissae/innervation ; Vibrissae/physiology
Language	English
Publishing date	2013-10-16
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2013.09.040
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Zs.A 2496: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 92: Show issues

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Article ; Online: VPS35 deficiency in the embryonic cortex leads to prenatal cell loss and abnormal development of axonal connectivity.

Roque, Micaela / Alves Rodrigues de Souza, Diego / Rangel-Sosa, Martha M / Altounian, Mike / Hocine, Mélanie / Deloulme, Jean-Christophe / Barbier, Emmanuel L / Mann, Fanny / Chauvet, Sophie

Molecular and cellular neurosciences

2022 Volume 120, Page(s) 103726

Abstract: VPS35 is a core component of the retromer complex involved in familial forms of neurodegenerative diseases such as Parkinson's and Alzheimer's disease. In mice, VPS35 is expressed during early brain development. However, previous studies have reported ... ...

Abstract	VPS35 is a core component of the retromer complex involved in familial forms of neurodegenerative diseases such as Parkinson's and Alzheimer's disease. In mice, VPS35 is expressed during early brain development. However, previous studies have reported that VPS35 activity is largely dispensable for normal neuronal development and initial elaboration of axonal projections. Here, we evaluated the role of VPS35 in the mouse embryonic brain using two Cre-driver lines that remove Vps35 from the cortex at different prenatal stages. We found that Vps35 mutant mice displayed microcephaly and decreased cortical thickness from the embryonic stages to adulthood. VPS35 also regulates cortical development by affecting a subpopulation of neural progenitor cells and the survival of postmitotic neurons. In addition, we showed that a lack of VPS35 leads to hypoplasia and misrouting of several axonal projections, including the anterior commissure and fornix. Furthermore, VPS35 deficiency impairs the non-autonomous development of thalamocortical axons (TCAs), which show severe disruption of innervation and terminal arborization in the cortex. Together, these data demonstrate that VPS35 plays a greater role in embryonic development of the mammalian brain than it was previously thought.
MeSH term(s)	Animals ; Axons/metabolism ; Mammals ; Mice ; Neurodegenerative Diseases/metabolism ; Neurogenesis ; Neurons/metabolism ; Vesicular Transport Proteins/metabolism
Chemical Substances	Vesicular Transport Proteins ; Vps35 protein, mouse
Language	English
Publishing date	2022-03-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1016/j.mcn.2022.103726
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Zs.A 3035: Show issues

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Article ; Online: An inverse stage-shift model to estimate the excess mortality and health economic impact of delayed access to cancer services due to the COVID-19 pandemic.

Degeling, Koen / Baxter, Nancy N / Emery, Jon / Jenkins, Mark A / Franchini, Fanny / Gibbs, Peter / Mann, G Bruce / McArthur, Grant / Solomon, Benjamin J / IJzerman, Maarten J

Asia-Pacific journal of clinical oncology

2021 Volume 17, Issue 4, Page(s) 359–367

Abstract: Aim: Decreased cancer incidence and reported changes to clinical management indicate that the COVID-19 pandemic has delayed cancer diagnosis and treatment. This study aimed to develop and apply a flexible model to estimate the impact of delayed ... ...

Abstract	Aim: Decreased cancer incidence and reported changes to clinical management indicate that the COVID-19 pandemic has delayed cancer diagnosis and treatment. This study aimed to develop and apply a flexible model to estimate the impact of delayed diagnosis and treatment on survival outcomes and healthcare costs based on a shift in the disease stage at treatment initiation. Methods: A model was developed and made publicly available to estimate population-level health economic outcomes by extrapolating and weighing stage-specific outcomes by the distribution of stages at treatment initiation. It was applied to estimate the impact of 3- and 6-month delays based on Australian data for stage I breast cancer, colorectal cancer, and lung cancer patients, and for T1 melanoma. Two approaches were explored to estimate stage shifts following a delay: (a) based on the relation between time to treatment initiation and overall survival (breast, colorectal, and lung cancer), and (b) based on the tumor growth rate (melanoma). Results: Using a conservative once-off 3-month delay and considering only shifts from stage I/T1 to stage II/T2, 88 excess deaths and $12 million excess healthcare costs were predicted in Australia over 5 years for all patients diagnosed in 2020. For a 6-month delay, excess mortality and healthcare costs were 349 deaths and $46 million over 5 years. Conclusions: The health and economic impacts of delays in treatment initiation cause an imminent policy concern. More accurate individual patient data on shifts in stage of disease during and after the COVID-19 pandemic are critical for further analyses.
MeSH term(s)	Australia/epidemiology ; Breast Neoplasms/mortality ; COVID-19 ; Colorectal Neoplasms/mortality ; Female ; Humans ; Lung Neoplasms/mortality ; Pandemics ; SARS-CoV-2
Language	English
Publishing date	2021-02-10
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2187409-8
ISSN	1743-7563 ; 1743-7555
ISSN (online)	1743-7563
ISSN	1743-7555
DOI	10.1111/ajco.13505
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Article ; Online: ARF1 prevents aberrant type I interferon induction by regulating STING activation and recycling.

Hirschenberger, Maximilian / Lepelley, Alice / Rupp, Ulrich / Klute, Susanne / Hunszinger, Victoria / Koepke, Lennart / Merold, Veronika / Didry-Barca, Blaise / Wondany, Fanny / Bergner, Tim / Moreau, Tatiana / Rodero, Mathieu P / Rösler, Reinhild / Wiese, Sebastian / Volpi, Stefano / Gattorno, Marco / Papa, Riccardo / Lynch, Sally-Ann / Haug, Marte G /

Houge, Gunnar / Wigby, Kristen M / Sprague, Jessica / Lenberg, Jerica / Read, Clarissa / Walther, Paul / Michaelis, Jens / Kirchhoff, Frank / de Oliveira Mann, Carina C / Crow, Yanick J / Sparrer, Konstantin M J

Nature communications

2023 Volume 14, Issue 1, Page(s) 6770

Abstract: Type I interferon (IFN) signalling is tightly controlled. Upon recognition of DNA by cyclic GMP-AMP synthase (cGAS), stimulator of interferon genes (STING) translocates along the endoplasmic reticulum (ER)-Golgi axis to induce IFN signalling. Termination ...

Abstract	Type I interferon (IFN) signalling is tightly controlled. Upon recognition of DNA by cyclic GMP-AMP synthase (cGAS), stimulator of interferon genes (STING) translocates along the endoplasmic reticulum (ER)-Golgi axis to induce IFN signalling. Termination is achieved through autophagic degradation or recycling of STING by retrograde Golgi-to-ER transport. Here, we identify the GTPase ADP-ribosylation factor 1 (ARF1) as a crucial negative regulator of cGAS-STING signalling. Heterozygous ARF1 missense mutations cause a previously unrecognized type I interferonopathy associated with enhanced IFN-stimulated gene expression. Disease-associated, GTPase-defective ARF1 increases cGAS-STING dependent type I IFN signalling in cell lines and primary patient cells. Mechanistically, mutated ARF1 perturbs mitochondrial morphology, causing cGAS activation by aberrant mitochondrial DNA release, and leads to accumulation of active STING at the Golgi/ERGIC due to defective retrograde transport. Our data show an unexpected dual role of ARF1 in maintaining cGAS-STING homeostasis, through promotion of mitochondrial integrity and STING recycling.
MeSH term(s)	Humans ; ADP-Ribosylation Factor 1/genetics ; ADP-Ribosylation Factor 1/metabolism ; Interferon Type I/metabolism ; Membrane Proteins/metabolism ; Nucleotidyltransferases/genetics ; Nucleotidyltransferases/metabolism ; Signal Transduction
Chemical Substances	ADP-Ribosylation Factor 1 (EC 3.6.5.2) ; Interferon Type I ; Membrane Proteins ; Nucleotidyltransferases (EC 2.7.7.-) ; STING1 protein, human ; ARF1 protein, human (EC 3.6.5.2)
Language	English
Publishing date	2023-11-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-42150-4
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