José Blanco-Ameijeiras

Institut de Biologia Molecular de Barcelona

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Elisa Martı́

Institut de Biologia Molecular de Barcelona

Elena Gonzalez-Gobartt

Institut de Biologia Molecular de Barcelona

Murielle Saade

Institut de Biologia Molecular de Barcelona

Guillaume Allio

Centre de Biologie du Développement

Bertrand Bénazéraf

Université Toulouse III - Paul Sabatier

Susana Usieto

Institut de Biologia Molecular de Barcelona

Diego S. Ferrero

Institut de Biologia Molecular de Barcelona

Santiago Ramón y Cajal

Vall d'Hebron Hospital Universitari

Núria Verdaguer

Consejo Superior de Investigaciones Científicas

Victor M. Ruiz-Arroyo

The University of Texas Southwestern Medical Center

Cooperative Institutions

Institut de Biologia Molecular de Barcelona

Consejo Superior de Investigaciones Científicas

Inserm

Centro Andaluz de Biología del Desarrollo

Centre de Biologie du Développement

Université de Toulouse

Université Toulouse III - Paul Sabatier

Centre National de la Recherche Scientifique

Université de Strasbourg

University of Pennsylvania

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Multimerization of Zika Virus-NS5 causes a ciliopathy and forces premature neurogenesis

bioRxiv (Cold Spring Harbor Laboratory) (2019)

Murielle Saade Diego S. Ferrero José Blanco-Ameijeiras Elena Gonzalez-Gobartt Victor M. Ruiz-Arroyo

Abstract Zika virus ( ZikV ) is a flavivirus that infects neural tissues, causing congenital microcephaly. ZikV has evolved multiple mechanisms to restrict proliferation and enhance cell death, although the underlying cellular events involved remain unclear. Here we show that the ZikV-NS5 protein interacts with host proteins at the base of the primary cilia in neural progenitor cells, causing an atypical non-genetic ciliopathy and premature neuron delamination. Furthermore, in human microcephalic fetal brain tissue, ZikV-NS5 persists at the base of the motile cilia in ependymal cells, which also exhibit a severe ciliopathy. While the enzymatic activity of ZikV-NS5 appears to be dispensable, the Y25, K28 and K29 residues in the protein, that are involved in NS5-oligomerization, are essential for the localization and interaction with components of the cilium base, promoting ciliopathy and premature neurogenesis. These findings lay the foundation to develop therapies that target ZikV-NS5-multimerization, preventing the developmental malformations associated with congenital Zika syndrome

Ciliopathy

Zika Virus

Microcephaly

Joubert syndrome

10.1101/719625

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Citations (2)

A centrosomal view of CNS growth

Development (2018)

Murielle Saade José Blanco-Ameijeiras Elena Gonzalez-Gobartt Elisa Martı́

ABSTRACT Embryonic development of the central nervous system (CNS) requires the proliferation of neural progenitor cells to be tightly regulated, allowing the formation of an organ with the right size and shape. This includes regulation of both the spatial distribution of mitosis and the mode of cell division. The centrosome, which is the main microtubule-organizing centre of animal cells, contributes to both of these processes. Here, we discuss the impact that centrosome-mediated control of cell division has on the shape of the overall growing CNS. We also review the intrinsic properties of the centrosome, both in terms of its molecular composition and its signalling capabilities, and discuss the fascinating notion that intrinsic centrosomal asymmetries in dividing neural progenitor cells are instructive for neurogenesis. Finally, we discuss the genetic links between centrosome dysfunction during development and the aetiology of microcephaly.

Centrosome cycle

Centriole

10.1242/dev.170613

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Citations (38)

Centrosome maturation – in tune with the cell cycle

Journal of Cell Science (2022)

José Blanco-Ameijeiras Pilar Lozano-Fernández Elisa Martı́

ABSTRACT Centrosomes are the main microtubule-organizing centres, playing essential roles in the organization of the cytoskeleton during interphase, and in the mitotic spindle, which controls chromosome segregation, during cell division. Centrosomes also act as the basal body of cilia, regulating cilium length and affecting extracellular signal reception as well as the integration of intracellular signalling pathways. Centrosomes are self-replicative and duplicate once every cell cycle to generate two centrosomes. The core support structure of the centrosome consists of two molecularly distinct centrioles. The mother (mature) centriole exhibits accessory appendages and is surrounded by both pericentriolar material and centriolar satellites, structures that the daughter (immature) centriole lacks. In this Review, we discuss what is currently known about centrosome duplication, its dialogue with the cell cycle and the sequential acquisition of specific components during centriole maturation. We also describe our current understanding of the mature centriolar structures that are required to build a cilium. Altogether, the built-in centrosome asymmetries that stem from the two centrosomes inheriting molecularly different centrioles sets the foundation for cell division being an intrinsically asymmetric process.

Centriole

Centrosome cycle

Basal body

Spindle pole body

Microtubule organizing center

Multipolar spindles

10.1242/jcs.259395

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Citations (36)

Multimerization of Zika Virus-NS5 Causes Ciliopathy and Forces Premature Neurogenesis

Cell stem cell (2020)

Murielle Saade Diego S. Ferrero José Blanco-Ameijeiras Elena Gonzalez-Gobartt Marco Flores‐Méndez

Ciliopathy

Zika Virus

Microcephaly

Joubert syndrome

10.1016/j.stem.2020.10.002

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Citations (31)

Cell intercalation driven by SMAD3 underlies secondary neural tube formation

Developmental Cell (2021)

Elena Gonzalez-Gobartt José Blanco-Ameijeiras Susana Usieto Guillaume Allio Bertrand Bénazéraf

Elongation

Lumen (anatomy)

10.1016/j.devcel.2021.03.023

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Citations (22)

Cell intercalation driven by SMAD3 underlies secondary neural tube formation

bioRxiv (Cold Spring Harbor Laboratory) (2020)

Elena Gonzalez-Gobartt José Blanco-Ameijeiras Susana Usieto Guillaume Allio Bertrand Bénazéraf

SUMMARY Body axis elongation is a hallmark of the vertebrate embryo, involving the architectural remodelling of the tailbud. Although it is clear how bi-potential neuro-mesodermal progenitors (NMPs) contribute to embryo elongation, the dynamic events that lead to de novo lumen formation and that culminate in the formation of a 3-Dimensional, secondary neural tube from NMPs, are poorly understood. Here, we used in vivo imaging of the chicken embryo to show that cell intercalation downstream of TGF-beta/SMAD3 signalling is required for secondary neural tube formation. Our analysis describes the initial events in embryo elongation including lineage restriction, the epithelial-to-mesenchymal transition of NMPs, and the initiation of lumen formation. Importantly, we show that the resolution of a single, centrally positioned continuous lumen, which occurs through the intercalation of central cells, requires SMAD3 activity. We anticipate that these findings will be relevant to understand caudal, skin-covered neural tube defects, amongst the most frequent birth defects detected in humans. HIGHLIGHTS . - Initiation of the lumen formation follows the acquisition of neural identity and epithelial polarization . . - Programmed cell death is not required for lumen resolution . . - Resolution of a single central lumen requires cell intercalation, driven by Smad3 activity . - The outcome of central cell division preceding cell intercalation, varies along the cranio-caudal axis .

Lumen (anatomy)

Elongation

10.1101/2020.08.24.261008

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Citations (2)

HUMAN SPINAL CORD ORGANOIDS REVEAL CELL INTERCALATION AS A CONSERVED MECHANISM FOR SECONDARY NEURULATION

bioRxiv (Cold Spring Harbor Laboratory) (2024)

José Blanco-Ameijeiras Mar García-Valero Yara El Majzoub Elena Rebollo Javier Macho‐Rendon

The spinal cord originates from bipotent stem cells called neuromesodermal progenitors, which are organized in a transient embryonic structure called the neural tube. The development of neural organoids is offering unprecedented tools to advance in the limited understanding of the initial construction and subsequent maturation of the human neural tube. In this study, we have generated human neural tube organoids with defined anterior and posterior identities. Through transcriptome profiling, we identified that the posterior organoids possessed a spinal cord identity. By modifying the culture conditions, we recapitulated the morphogenetic events for secondary neurulation in vivo, and revealed that de novo lumen formation in the spinal cord organoids involves a conserved Yap-dependent cell intercalation process. We believe that these findings will contribute to our understanding of the mechanisms required for building the human spinal cord in the embryo, and to understand the biological basis of neurodevelopmental disorders, which are among the most common birth defects.

Organoid

Neurulation

10.1101/2024.11.19.624296

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Citations (1)