The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression
- Autores
- Whittaker, Danielle E.; Riegman, Kimberley L. H.; Kasah, Sahrunizam; Mohan, Conor; Yu, Tian; Sala, Blanca Pijuan; Hebaishi, Husam; Caruso, Angela; Marques, Ana Claudia; Michetti, Caterina; Sanz Smachetti, María Eugenia; Shah, Apar; Sabbioni, Mara; Kulhanci, Omer; Tee, Wee-Wei; Reinberg, Danny; Scattoni, Maria Luisa; Volk, Holger; McGonnell, Imelda; Wardle, Fiona C.; Fernandez, Cathy; Basson, Albert
- Año de publicación
- 2017
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- The mechanisms underlying the neurodevelopmental deficits associated with CHARGE syndrome, which include cerebellar hypoplasia, developmental delay, coordination problems, and autistic features, have not been identified. CHARGE syndrome has been associated with mutations in the gene encoding the ATP-dependent chromatin remodeler CHD7. CHD7 is expressed in neural stem and progenitor cells, but its role in neurogenesis during brain development remains unknown. Here we have shown that deletion of Chd7 from cerebellar granule cell progenitors (GCps) results in reduced GCp proliferation, cerebellar hypoplasia, developmental delay, and motor deficits in mice. Genome-wide expression profiling revealed downregulated expression of the gene encoding the glycoprotein reelin (Reln) in Chd7-deficient GCps. Recessive RELN mutations have been associated with severe cerebellar hypoplasia in humans. We found molecular and genetic evidence that reductions in Reln expression contribute to GCp proliferative defects and cerebellar hypoplasia in GCp-specific Chd7 mouse mutants. Finally, we showed that CHD7 is necessary for maintaining an open, accessible chromatin state at the Reln locus. Taken together, this study shows that Reln gene expression is regulated by chromatin remodeling, identifies CHD7 as a previously unrecognized upstream regulator of Reln, and provides direct in vivo evidence that a mammalian CHD protein can control brain development by modulating chromatin accessibility in neuronal progenitors.
Fil: Whittaker, Danielle E.. Royal Veterinary College University Of London; . King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido
Fil: Riegman, Kimberley L. H.. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido
Fil: Kasah, Sahrunizam. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido
Fil: Mohan, Conor. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido
Fil: Yu, Tian. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido
Fil: Sala, Blanca Pijuan. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido
Fil: Hebaishi, Husam. University College London; Estados Unidos
Fil: Caruso, Angela. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; Italia
Fil: Marques, Ana Claudia. University of Oxford. Department of Physiology, Anatomy and Genetics; Reino Unido
Fil: Michetti, Caterina. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; Italia
Fil: Sanz Smachetti, María Eugenia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mar del Plata. Instituto de Investigaciones En Biodiversidad y Biotecnología; Argentina. Fundación para Investigaciones Biológicas Aplicadas; Argentina
Fil: Shah, Apar. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido
Fil: Sabbioni, Mara. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; Italia
Fil: Kulhanci, Omer. King’s College London, London, United Kingdom. Institute of Psychiatry, Psychology & Neuroscience. MRC Social, Genetic & Developmental Psychiatry Centre; Reino Unido
Fil: Tee, Wee-Wei. New York University School of Medicine. Department of Molecular Pharmacology and Biochemistry. Howard Hughes Medical Institute; Estados Unidos
Fil: Reinberg, Danny. New York University School of Medicine. Department of Molecular Pharmacology and Biochemistry. Howard Hughes Medical Institute; Estados Unidos
Fil: Scattoni, Maria Luisa. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; Italia
Fil: Volk, Holger. Royal Veterinary College University Of London; Reino Unido
Fil: McGonnell, Imelda. Royal Veterinary College University Of London; Reino Unido
Fil: Wardle, Fiona C.. King’s College London. Randall Division; Reino Unido
Fil: Fernandez, Cathy. King’s College London, London, United Kingdom. Psychology & Neuroscience; Reino Unido
Fil: Basson, Albert. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido - Materia
-
CHD7
cerebellar development
reelin expresion - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/19973
Ver los metadatos del registro completo
| id |
CONICETDig_0f8a66479ae0a80b0f7697a902268b9f |
|---|---|
| oai_identifier_str |
oai:ri.conicet.gov.ar:11336/19973 |
| network_acronym_str |
CONICETDig |
| repository_id_str |
3498 |
| network_name_str |
CONICET Digital (CONICET) |
| spelling |
The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expressionWhittaker, Danielle E.Riegman, Kimberley L. H.Kasah, SahrunizamMohan, ConorYu, TianSala, Blanca PijuanHebaishi, HusamCaruso, AngelaMarques, Ana ClaudiaMichetti, CaterinaSanz Smachetti, María EugeniaShah, AparSabbioni, MaraKulhanci, OmerTee, Wee-WeiReinberg, DannyScattoni, Maria LuisaVolk, HolgerMcGonnell, ImeldaWardle, Fiona C.Fernandez, CathyBasson, AlbertCHD7cerebellar developmentreelin expresionhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The mechanisms underlying the neurodevelopmental deficits associated with CHARGE syndrome, which include cerebellar hypoplasia, developmental delay, coordination problems, and autistic features, have not been identified. CHARGE syndrome has been associated with mutations in the gene encoding the ATP-dependent chromatin remodeler CHD7. CHD7 is expressed in neural stem and progenitor cells, but its role in neurogenesis during brain development remains unknown. Here we have shown that deletion of Chd7 from cerebellar granule cell progenitors (GCps) results in reduced GCp proliferation, cerebellar hypoplasia, developmental delay, and motor deficits in mice. Genome-wide expression profiling revealed downregulated expression of the gene encoding the glycoprotein reelin (Reln) in Chd7-deficient GCps. Recessive RELN mutations have been associated with severe cerebellar hypoplasia in humans. We found molecular and genetic evidence that reductions in Reln expression contribute to GCp proliferative defects and cerebellar hypoplasia in GCp-specific Chd7 mouse mutants. Finally, we showed that CHD7 is necessary for maintaining an open, accessible chromatin state at the Reln locus. Taken together, this study shows that Reln gene expression is regulated by chromatin remodeling, identifies CHD7 as a previously unrecognized upstream regulator of Reln, and provides direct in vivo evidence that a mammalian CHD protein can control brain development by modulating chromatin accessibility in neuronal progenitors.Fil: Whittaker, Danielle E.. Royal Veterinary College University Of London; . King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino UnidoFil: Riegman, Kimberley L. H.. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino UnidoFil: Kasah, Sahrunizam. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino UnidoFil: Mohan, Conor. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino UnidoFil: Yu, Tian. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino UnidoFil: Sala, Blanca Pijuan. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino UnidoFil: Hebaishi, Husam. University College London; Estados UnidosFil: Caruso, Angela. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; ItaliaFil: Marques, Ana Claudia. University of Oxford. Department of Physiology, Anatomy and Genetics; Reino UnidoFil: Michetti, Caterina. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; ItaliaFil: Sanz Smachetti, María Eugenia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mar del Plata. Instituto de Investigaciones En Biodiversidad y Biotecnología; Argentina. Fundación para Investigaciones Biológicas Aplicadas; ArgentinaFil: Shah, Apar. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino UnidoFil: Sabbioni, Mara. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; ItaliaFil: Kulhanci, Omer. King’s College London, London, United Kingdom. Institute of Psychiatry, Psychology & Neuroscience. MRC Social, Genetic & Developmental Psychiatry Centre; Reino UnidoFil: Tee, Wee-Wei. New York University School of Medicine. Department of Molecular Pharmacology and Biochemistry. Howard Hughes Medical Institute; Estados UnidosFil: Reinberg, Danny. New York University School of Medicine. Department of Molecular Pharmacology and Biochemistry. Howard Hughes Medical Institute; Estados UnidosFil: Scattoni, Maria Luisa. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; ItaliaFil: Volk, Holger. Royal Veterinary College University Of London; Reino UnidoFil: McGonnell, Imelda. Royal Veterinary College University Of London; Reino UnidoFil: Wardle, Fiona C.. King’s College London. Randall Division; Reino UnidoFil: Fernandez, Cathy. King’s College London, London, United Kingdom. Psychology & Neuroscience; Reino UnidoFil: Basson, Albert. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino UnidoAmer Soc Clinical Investigation Inc2017-03-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/19973Whittaker, Danielle E.; Riegman, Kimberley L. H.; Kasah, Sahrunizam; Mohan, Conor; Yu, Tian; et al.; The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression; Amer Soc Clinical Investigation Inc; Journal Of Clinical Investigation; 127; 3; 1-3-2017; 874-8870021-9738CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1172/JCI83408info:eu-repo/semantics/altIdentifier/url/https://www.jci.org/articles/view/83408info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:58:09Zoai:ri.conicet.gov.ar:11336/19973instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:58:09.74CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression |
| title |
The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression |
| spellingShingle |
The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression Whittaker, Danielle E. CHD7 cerebellar development reelin expresion |
| title_short |
The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression |
| title_full |
The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression |
| title_fullStr |
The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression |
| title_full_unstemmed |
The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression |
| title_sort |
The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression |
| dc.creator.none.fl_str_mv |
Whittaker, Danielle E. Riegman, Kimberley L. H. Kasah, Sahrunizam Mohan, Conor Yu, Tian Sala, Blanca Pijuan Hebaishi, Husam Caruso, Angela Marques, Ana Claudia Michetti, Caterina Sanz Smachetti, María Eugenia Shah, Apar Sabbioni, Mara Kulhanci, Omer Tee, Wee-Wei Reinberg, Danny Scattoni, Maria Luisa Volk, Holger McGonnell, Imelda Wardle, Fiona C. Fernandez, Cathy Basson, Albert |
| author |
Whittaker, Danielle E. |
| author_facet |
Whittaker, Danielle E. Riegman, Kimberley L. H. Kasah, Sahrunizam Mohan, Conor Yu, Tian Sala, Blanca Pijuan Hebaishi, Husam Caruso, Angela Marques, Ana Claudia Michetti, Caterina Sanz Smachetti, María Eugenia Shah, Apar Sabbioni, Mara Kulhanci, Omer Tee, Wee-Wei Reinberg, Danny Scattoni, Maria Luisa Volk, Holger McGonnell, Imelda Wardle, Fiona C. Fernandez, Cathy Basson, Albert |
| author_role |
author |
| author2 |
Riegman, Kimberley L. H. Kasah, Sahrunizam Mohan, Conor Yu, Tian Sala, Blanca Pijuan Hebaishi, Husam Caruso, Angela Marques, Ana Claudia Michetti, Caterina Sanz Smachetti, María Eugenia Shah, Apar Sabbioni, Mara Kulhanci, Omer Tee, Wee-Wei Reinberg, Danny Scattoni, Maria Luisa Volk, Holger McGonnell, Imelda Wardle, Fiona C. Fernandez, Cathy Basson, Albert |
| author2_role |
author author author author author author author author author author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
CHD7 cerebellar development reelin expresion |
| topic |
CHD7 cerebellar development reelin expresion |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
| dc.description.none.fl_txt_mv |
The mechanisms underlying the neurodevelopmental deficits associated with CHARGE syndrome, which include cerebellar hypoplasia, developmental delay, coordination problems, and autistic features, have not been identified. CHARGE syndrome has been associated with mutations in the gene encoding the ATP-dependent chromatin remodeler CHD7. CHD7 is expressed in neural stem and progenitor cells, but its role in neurogenesis during brain development remains unknown. Here we have shown that deletion of Chd7 from cerebellar granule cell progenitors (GCps) results in reduced GCp proliferation, cerebellar hypoplasia, developmental delay, and motor deficits in mice. Genome-wide expression profiling revealed downregulated expression of the gene encoding the glycoprotein reelin (Reln) in Chd7-deficient GCps. Recessive RELN mutations have been associated with severe cerebellar hypoplasia in humans. We found molecular and genetic evidence that reductions in Reln expression contribute to GCp proliferative defects and cerebellar hypoplasia in GCp-specific Chd7 mouse mutants. Finally, we showed that CHD7 is necessary for maintaining an open, accessible chromatin state at the Reln locus. Taken together, this study shows that Reln gene expression is regulated by chromatin remodeling, identifies CHD7 as a previously unrecognized upstream regulator of Reln, and provides direct in vivo evidence that a mammalian CHD protein can control brain development by modulating chromatin accessibility in neuronal progenitors. Fil: Whittaker, Danielle E.. Royal Veterinary College University Of London; . King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido Fil: Riegman, Kimberley L. H.. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido Fil: Kasah, Sahrunizam. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido Fil: Mohan, Conor. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido Fil: Yu, Tian. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido Fil: Sala, Blanca Pijuan. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido Fil: Hebaishi, Husam. University College London; Estados Unidos Fil: Caruso, Angela. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; Italia Fil: Marques, Ana Claudia. University of Oxford. Department of Physiology, Anatomy and Genetics; Reino Unido Fil: Michetti, Caterina. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; Italia Fil: Sanz Smachetti, María Eugenia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mar del Plata. Instituto de Investigaciones En Biodiversidad y Biotecnología; Argentina. Fundación para Investigaciones Biológicas Aplicadas; Argentina Fil: Shah, Apar. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido Fil: Sabbioni, Mara. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; Italia Fil: Kulhanci, Omer. King’s College London, London, United Kingdom. Institute of Psychiatry, Psychology & Neuroscience. MRC Social, Genetic & Developmental Psychiatry Centre; Reino Unido Fil: Tee, Wee-Wei. New York University School of Medicine. Department of Molecular Pharmacology and Biochemistry. Howard Hughes Medical Institute; Estados Unidos Fil: Reinberg, Danny. New York University School of Medicine. Department of Molecular Pharmacology and Biochemistry. Howard Hughes Medical Institute; Estados Unidos Fil: Scattoni, Maria Luisa. Istituto Superiore di Sanità. Department of Cell Biology and Neuroscience. Neurotoxicology and Neuroendocrinology Section; Italia Fil: Volk, Holger. Royal Veterinary College University Of London; Reino Unido Fil: McGonnell, Imelda. Royal Veterinary College University Of London; Reino Unido Fil: Wardle, Fiona C.. King’s College London. Randall Division; Reino Unido Fil: Fernandez, Cathy. King’s College London, London, United Kingdom. Psychology & Neuroscience; Reino Unido Fil: Basson, Albert. King’s College London. Department of Craniofacial Development and Stem Cell Biology. Guy’s Hospital Tower Wing; Reino Unido |
| description |
The mechanisms underlying the neurodevelopmental deficits associated with CHARGE syndrome, which include cerebellar hypoplasia, developmental delay, coordination problems, and autistic features, have not been identified. CHARGE syndrome has been associated with mutations in the gene encoding the ATP-dependent chromatin remodeler CHD7. CHD7 is expressed in neural stem and progenitor cells, but its role in neurogenesis during brain development remains unknown. Here we have shown that deletion of Chd7 from cerebellar granule cell progenitors (GCps) results in reduced GCp proliferation, cerebellar hypoplasia, developmental delay, and motor deficits in mice. Genome-wide expression profiling revealed downregulated expression of the gene encoding the glycoprotein reelin (Reln) in Chd7-deficient GCps. Recessive RELN mutations have been associated with severe cerebellar hypoplasia in humans. We found molecular and genetic evidence that reductions in Reln expression contribute to GCp proliferative defects and cerebellar hypoplasia in GCp-specific Chd7 mouse mutants. Finally, we showed that CHD7 is necessary for maintaining an open, accessible chromatin state at the Reln locus. Taken together, this study shows that Reln gene expression is regulated by chromatin remodeling, identifies CHD7 as a previously unrecognized upstream regulator of Reln, and provides direct in vivo evidence that a mammalian CHD protein can control brain development by modulating chromatin accessibility in neuronal progenitors. |
| publishDate |
2017 |
| dc.date.none.fl_str_mv |
2017-03-01 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
| format |
article |
| status_str |
publishedVersion |
| dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/19973 Whittaker, Danielle E.; Riegman, Kimberley L. H.; Kasah, Sahrunizam; Mohan, Conor; Yu, Tian; et al.; The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression; Amer Soc Clinical Investigation Inc; Journal Of Clinical Investigation; 127; 3; 1-3-2017; 874-887 0021-9738 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/19973 |
| identifier_str_mv |
Whittaker, Danielle E.; Riegman, Kimberley L. H.; Kasah, Sahrunizam; Mohan, Conor; Yu, Tian; et al.; The chromatin remodeling factor CHD7 controls cerebellar development by regulating reelin expression; Amer Soc Clinical Investigation Inc; Journal Of Clinical Investigation; 127; 3; 1-3-2017; 874-887 0021-9738 CONICET Digital CONICET |
| dc.language.none.fl_str_mv |
eng |
| language |
eng |
| dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1172/JCI83408 info:eu-repo/semantics/altIdentifier/url/https://www.jci.org/articles/view/83408 |
| dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
| eu_rights_str_mv |
openAccess |
| rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
| dc.format.none.fl_str_mv |
application/pdf application/pdf |
| dc.publisher.none.fl_str_mv |
Amer Soc Clinical Investigation Inc |
| publisher.none.fl_str_mv |
Amer Soc Clinical Investigation Inc |
| dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
| reponame_str |
CONICET Digital (CONICET) |
| collection |
CONICET Digital (CONICET) |
| instname_str |
Consejo Nacional de Investigaciones Científicas y Técnicas |
| repository.name.fl_str_mv |
CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
| repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
| _version_ |
1842269504216760320 |
| score |
13.13397 |