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Article: Editorial: Bench to bedside: translating pre-clinical research into clinical trials for childhood brain tumors.

Endersby, Raelene / Wainwright, Brandon J / Gottardo, Nicholas G

2023 Volume 13, Page(s) 1274465

Language	English
Publishing date	2023-08-17
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2023.1274465
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Article ; Online: Elongator and the role of its subcomplexes in human diseases.

Gaik, Monika / Kojic, Marija / Wainwright, Brandon J / Glatt, Sebastian

EMBO molecular medicine

2022 Volume 15, Issue 2, Page(s) e16418

Abstract: The Elongator complex was initially identified in yeast, and a variety of distinct cellular functions have been assigned to the complex. In the last decade, several research groups focussed on dissecting its structure, tRNA modification activity and role ...

Abstract	The Elongator complex was initially identified in yeast, and a variety of distinct cellular functions have been assigned to the complex. In the last decade, several research groups focussed on dissecting its structure, tRNA modification activity and role in translation regulation. Recently, Elongator emerged as a crucial factor for various human diseases, and its involvement has triggered a strong interest in the complex from numerous clinical groups. The Elongator complex is highly conserved among eukaryotes, with all six subunits (Elp1-6) contributing to its stability and function. Yet, recent studies have shown that the two subcomplexes, namely the catalytic Elp123 and accessory Elp456, may have distinct roles in the development of different neuronal subtypes. This Commentary aims to provide a brief overview and new perspectives for more systematic efforts to explore the functions of the Elongator in health and disease.
MeSH term(s)	Humans ; Protein Subunits/chemistry ; Protein Subunits/genetics ; Saccharomyces cerevisiae/genetics
Chemical Substances	Protein Subunits
Language	English
Publishing date	2022-11-30
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.202216418
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Zs.A 6784: Show issues

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Article ; Online: Patched1 patterns Fibroblast growth factor 10 and Forkhead box F1 expression during pulmonary branch formation.

Ho, Uda Y / Wainwright, Brandon J

Mechanisms of development

2017 Volume 147, Page(s) 37–48

Abstract: Hedgehog (Hh) signalling, Fibroblast growth factor 10 (Fgf10) and Forkhead box F1 (Foxf1) are each individually important for directing pulmonary branch formation but their interactions are not well understood. Here we demonstrate that Hh signalling is ... ...

Abstract	Hedgehog (Hh) signalling, Fibroblast growth factor 10 (Fgf10) and Forkhead box F1 (Foxf1) are each individually important for directing pulmonary branch formation but their interactions are not well understood. Here we demonstrate that Hh signalling is vital in regulating Foxf1 and Fgf10 expression during branching. The Hedgehog receptor Patched1 (Ptch1) was conditionally inactivated in the lung mesenchyme by Dermo1-Cre in vivo or using a recombinant Cre recombinase protein (HNCre) in lung cultures resulting in cell autonomous activation of Hh signalling. Homozygous mesenchymal Ptch1 deleted embryos (Dermo1Cre+/-;Ptch1
MeSH term(s)	Animals ; Fibroblast Growth Factor 10/genetics ; Fibroblast Growth Factor 10/metabolism ; Fibroblast Growth Factor 10/pharmacology ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Gene Expression Regulation, Developmental ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Integrases/genetics ; Integrases/metabolism ; Lung/drug effects ; Lung/growth & development ; Lung/metabolism ; Mice ; Mice, Transgenic ; Organ Culture Techniques ; Organogenesis/drug effects ; Organogenesis/genetics ; Patched-1 Receptor/deficiency ; Patched-1 Receptor/genetics ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction
Chemical Substances	Fgf10 protein, mouse ; Fibroblast Growth Factor 10 ; Forkhead Transcription Factors ; Foxf1a protein, mouse ; Hedgehog Proteins ; Patched-1 Receptor ; Ptch1 protein, mouse ; Recombinant Proteins ; Shh protein, mouse ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2017-09-20
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1055986-3
ISSN	1872-6356 ; 0925-4773
ISSN (online)	1872-6356
ISSN	0925-4773
DOI	10.1016/j.mod.2017.09.001
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Zs.A 1152: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Genetic and functional interaction network analysis reveals global enrichment of regulatory T cell genes influencing basal cell carcinoma susceptibility.

Adolphe, Christelle / Xue, Angli / Fard, Atefeh Taherian / Genovesi, Laura A / Yang, Jian / Wainwright, Brandon J

Genome medicine

2021 Volume 13, Issue 1, Page(s) 19

Abstract: Background: Basal cell carcinoma (BCC) of the skin is the most common form of human cancer, with more than 90% of tumours presenting with clear genetic activation of the Hedgehog pathway. However, polygenic risk factors affecting mechanisms such as DNA ... ...

Abstract	Background: Basal cell carcinoma (BCC) of the skin is the most common form of human cancer, with more than 90% of tumours presenting with clear genetic activation of the Hedgehog pathway. However, polygenic risk factors affecting mechanisms such as DNA repair and cell cycle checkpoints or which modulate the tumour microenvironment or host immune system play significant roles in determining whether genetic mutations culminate in BCC development. We set out to define background genetic factors that play a role in influencing BCC susceptibility via promoting or suppressing the effects of oncogenic drivers of BCC. Methods: We performed genome-wide association studies (GWAS) on 17,416 cases and 375,455 controls. We subsequently performed statistical analysis by integrating data from population-based genetic studies of multi-omics data, including blood- and skin-specific expression quantitative trait loci and methylation quantitative trait loci, thereby defining a list of functionally relevant candidate BCC susceptibility genes from our GWAS loci. We also constructed a local GWAS functional interaction network (consisting of GWAS nearest genes) and another functional interaction network, consisting specifically of candidate BCC susceptibility genes. Results: A total of 71 GWAS loci and 46 functional candidate BCC susceptibility genes were identified. Increased risk of BCC was associated with the decreased expression of 26 susceptibility genes and increased expression of 20 susceptibility genes. Pathway analysis of the functional candidate gene regulatory network revealed strong enrichment for cell cycle, cell death, and immune regulation processes, with a global enrichment of genes and proteins linked to T Conclusions: Our genome-wide association analyses and functional interaction network analysis reveal an enrichment of risk variants that function in an immunosuppressive regulatory network, likely hindering cancer immune surveillance and effective antitumour immunity.
MeSH term(s)	Biological Specimen Banks ; Carcinoma, Basal Cell/blood ; Carcinoma, Basal Cell/genetics ; Carcinoma, Basal Cell/immunology ; DNA Methylation/genetics ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Mendelian Randomization Analysis ; Organ Specificity/genetics ; Protein Interaction Maps/genetics ; Quantitative Trait Loci/genetics ; Skin Neoplasms/blood ; Skin Neoplasms/genetics ; Skin Neoplasms/immunology ; T-Lymphocytes, Regulatory/immunology
Language	English
Publishing date	2021-02-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-021-00827-9
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Article ; Online: MicroRNAs Promote Granule Cell Expansion in the Cerebellum Through Gli2.

Constantin, Lena / Wainwright, Brandon J

Cerebellum (London, England)

2015 Volume 14, Issue 6, Page(s) 688–698

Abstract: MicroRNAs (miRNAs) are important regulators of cerebellar function and homeostasis. Their deregulation results in cerebellar neuronal degeneration and spinocerebellar ataxia type 1 and contributes to medulloblastoma. Canonical miRNA processing involves ... ...

Abstract	MicroRNAs (miRNAs) are important regulators of cerebellar function and homeostasis. Their deregulation results in cerebellar neuronal degeneration and spinocerebellar ataxia type 1 and contributes to medulloblastoma. Canonical miRNA processing involves Dicer, which cleaves precursor miRNAs into mature double-stranded RNA duplexes. In order to address the role of miRNAs in cerebellar granule cell precursor development, loxP-flanked exons of Dicer1 were conditionally inactivated using the granule cell precursor-specific Atoh1-Cre recombinase. A reduction of 87% in Dicer1 transcript was achieved in this conditional Dicer knockdown model. Although knockdown resulted in normal survival, mice had disruptions to the cortical layering of the anterior cerebellum, which resulted from the premature differentiation of granule cell precursors in this region during neonatal development. This defect manifested as a thinner external granular layer with ectopic mature granule cells, and a depleted internal granular layer. We found that expression of the activator components of the Hedgehog-Patched pathway, the Gli family of transcription factors, was perturbed in conditional Dicer knockdown mice. We propose that loss of Gli2 mRNA mediated the anterior-restricted defect in conditional Dicer knockdown mice and, as proof of principle, were able to show that miR-106b positively regulated Gli2 mRNA expression. These findings confirm the importance of miRNAs as positive mediators of Hedgehog-Patched signalling during granule cell precursor development.
MeSH term(s)	Animals ; Cerebellum/growth & development ; Cerebellum/pathology ; Cerebellum/physiology ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/metabolism ; Gene Knockdown Techniques ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Mice, Transgenic ; MicroRNAs/metabolism ; Neural Stem Cells/pathology ; Neural Stem Cells/physiology ; Neurogenesis/physiology ; Neurons/pathology ; Neurons/physiology ; Organ Size ; Phenotype ; RNA, Messenger/metabolism ; Ribonuclease III/genetics ; Ribonuclease III/metabolism ; Zinc Finger Protein Gli2
Chemical Substances	Gli2 protein, mouse ; Kruppel-Like Transcription Factors ; MicroRNAs ; Mirn106 microRNA, mouse ; RNA, Messenger ; Zinc Finger Protein Gli2 ; Dicer1 protein, mouse (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2015-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2112586-7
ISSN	1473-4230 ; 1473-4222
ISSN (online)	1473-4230
ISSN	1473-4222
DOI	10.1007/s12311-015-0672-x
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Zs.A 5795: Show issues

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Article ; Online: A novel ELP1 mutation impairs the function of the Elongator complex and causes a severe neurodevelopmental phenotype.

Kojic, Marija / Abbassi, Nour E H / Lin, Ting-Yu / Jones, Alun / Wakeling, Emma L / Clement, Emma / Nakou, Vasiliki / Singleton, Matthew / Dobosz, Dominika / Kaliakatsos, Marios / Glatt, Sebastian / Wainwright, Brandon J

Journal of human genetics

2023 Volume 68, Issue 7, Page(s) 445–453

Abstract: Background: Neurodevelopmental disorders (NDDs) are heterogeneous, debilitating conditions that include motor and cognitive disability and social deficits. The genetic factors underlying the complex phenotype of NDDs remain to be elucidated. ... ...

Abstract	Background: Neurodevelopmental disorders (NDDs) are heterogeneous, debilitating conditions that include motor and cognitive disability and social deficits. The genetic factors underlying the complex phenotype of NDDs remain to be elucidated. Accumulating evidence suggest that the Elongator complex plays a role in NDDs, given that patient-derived mutations in its ELP2, ELP3, ELP4 and ELP6 subunits have been associated with these disorders. Pathogenic variants in its largest subunit ELP1 have been previously found in familial dysautonomia and medulloblastoma, with no link to NDDs affecting primarily the central nervous system. Methods: Clinical investigation included patient history and physical, neurological and magnetic resonance imaging (MRI) examination. A novel homozygous likely pathogenic ELP1 variant was identified by whole-genome sequencing. Functional studies included in silico analysis of the mutated ELP1 in the context of the holo-complex, production and purification of the ELP1 harbouring the identified mutation and in vitro analyses using microscale thermophoresis for tRNA binding assay and acetyl-CoA hydrolysis assay. Patient fibroblasts were harvested for tRNA modification analysis using HPLC coupled to mass spectrometry. Results: We report a novel missense mutation in the ELP1 identified in two siblings with intellectual disability and global developmental delay. We show that the mutation perturbs the ability of ELP123 to bind tRNAs and compromises the function of the Elongator in vitro and in human cells. Conclusion: Our study expands the mutational spectrum of ELP1 and its association with different neurodevelopmental conditions and provides a specific target for genetic counselling.
MeSH term(s)	Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Mutation ; Mutation, Missense ; Nerve Tissue Proteins/genetics ; Phenotype ; RNA, Transfer/metabolism ; Transcriptional Elongation Factors/genetics ; Neurodevelopmental Disorders/genetics
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Nerve Tissue Proteins ; RNA, Transfer (9014-25-9) ; Elp1 protein, human ; Transcriptional Elongation Factors
Language	English
Publishing date	2023-03-02
Publishing country	England
Document type	Journal Article
ZDB-ID	1425192-9
ISSN	1435-232X ; 1434-5161
ISSN (online)	1435-232X
ISSN	1434-5161
DOI	10.1038/s10038-023-01135-3
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Zs.A 201: Show issues

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Article ; Online: Efficient detection and monitoring of pediatric brain malignancies with liquid biopsy based on patient-specific somatic mutation screening.

Kojic, Marija / Maybury, Mellissa K / Waddell, Nicola / Koufariotis, Lambros T / Addala, Venkateswar / Millar, Amanda / Wood, Scott / Pearson, John V / Hansford, Jordan R / Hassall, Tim / Wainwright, Brandon J

Neuro-oncology

2023 Volume 25, Issue 8, Page(s) 1507–1517

Abstract: Background: Brain cancer is the leading cause of cancer-related death in children. Early detection and serial monitoring are essential for better therapeutic outcomes. Liquid biopsy has recently emerged as a promising approach for detecting these tumors ...

Abstract	Background: Brain cancer is the leading cause of cancer-related death in children. Early detection and serial monitoring are essential for better therapeutic outcomes. Liquid biopsy has recently emerged as a promising approach for detecting these tumors by screening body fluids for the presence of circulating tumor DNA (ctDNA). Here we tested the limits of liquid biopsy using patient-specific somatic mutations to detect and monitor primary and metastatic pediatric brain cancer. Methods: Somatic mutations were identified in 3 ependymoma, 1 embryonal tumor with multilayered rosettes, 1 central nervous system neuroblastoma, and 7 medulloblastoma patients. The mutations were used as liquid biomarkers for serial assessment of cerebrospinal fluid (CSF) samples using a droplet digital PCR (ddPCR) system. The findings were correlated to the imaging data and clinical assessment to evaluate the utility of the approach for clinical translation. Results: We developed personalized somatic mutation ddPCR assays which we show are highly specific, sensitive, and efficient in detection and monitoring of ctDNA, with a positive correlation between presence of ctDNA, disease course, and clinical outcomes in the majority of patients. Conclusions: We demonstrate the feasibility and clinical utility of personalized mutation-based liquid biopsy for the surveillance of brain cancer in children. However, even with this specific and sensitive approach, we identified some potential false negative analyses. Overall, our results indicate that changes in ctDNA profiles over time demonstrate the great potential of our specific approach for predicting tumor progression, burden, and response to treatment.
MeSH term(s)	Humans ; Child ; Biomarkers, Tumor/genetics ; Brain Neoplasms/diagnosis ; Brain Neoplasms/genetics ; Liquid Biopsy/methods ; Circulating Tumor DNA/genetics ; Mutation
Chemical Substances	Biomarkers, Tumor ; Circulating Tumor DNA
Language	English
Publishing date	2023-02-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2028601-6
ISSN	1523-5866 ; 1522-8517
ISSN (online)	1523-5866
ISSN	1522-8517
DOI	10.1093/neuonc/noad032
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Zs.A 5307: Show issues

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Article ; Online: MicroRNA Biogenesis and Hedgehog-Patched Signaling Cooperate to Regulate an Important Developmental Transition in Granule Cell Development.

Constantin, Lena / Constantin, Myrna / Wainwright, Brandon J

Genetics

2016 Volume 202, Issue 3, Page(s) 1105–1118

Abstract: The Dicer1, Dcr-1 homolog (Drosophila) gene encodes a type III ribonuclease required for the canonical maturation and functioning of microRNAs (miRNAs). Subsets of miRNAs are known to regulate normal cerebellar granule cell development, in addition to ... ...

Abstract	The Dicer1, Dcr-1 homolog (Drosophila) gene encodes a type III ribonuclease required for the canonical maturation and functioning of microRNAs (miRNAs). Subsets of miRNAs are known to regulate normal cerebellar granule cell development, in addition to the growth and progression of medulloblastoma, a neoplasm that often originates from granule cell precursors. Multiple independent studies have also demonstrated that deregulation of Sonic Hedgehog (Shh)-Patched (Ptch) signaling, through miRNAs, is causative of granule cell pathologies. In the present study, we investigated the genetic interplay between miRNA biogenesis and Shh-Ptch signaling in granule cells of the cerebellum by way of the Cre/lox recombination system in genetically engineered models of Mus musculus (mouse). We demonstrate that, although the miRNA biogenesis and Shh-Ptch-signaling pathways, respectively, regulate the opposing growth processes of cerebellar hypoplasia and hyperplasia leading to medulloblastoma, their concurrent deregulation was nonadditive and did not bring the growth phenotypes toward an expected equilibrium. Instead, mice developed either hypoplasia or medulloblastoma, but of a greater severity. Furthermore, some genotypes were bistable, whereby subsets of mice developed hypoplasia or medulloblastoma. This implies that miRNAs and Shh-Ptch signaling regulate an important developmental transition in granule cells of the cerebellum. We also conclusively show that the Dicer1 gene encodes a haploinsufficient tumor suppressor gene for Ptch1-induced medulloblastoma, with the monoallielic loss of Dicer1 more severe than biallelic loss. These findings exemplify how genetic interplay between pathways may produce nonadditive effects with a substantial and unpredictable impact on biology. Furthermore, these findings suggest that the functional dosage of Dicer1 may nonadditively influence a wide range of Shh-Ptch-dependent pathologies.
MeSH term(s)	Animals ; Cell Line, Tumor ; Cerebellum/abnormalities ; Cerebellum/cytology ; Cerebellum/pathology ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/physiology ; Developmental Disabilities/pathology ; Gene Dosage ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Genes, Tumor Suppressor ; Hedgehog Proteins/physiology ; Medulloblastoma/pathology ; Mice ; Mice, Transgenic ; MicroRNAs/physiology ; Nervous System Malformations/pathology ; Neurons/cytology ; Patched-1 Receptor/physiology ; Protein Isoforms/genetics ; Protein Isoforms/physiology ; Ribonuclease III/genetics ; Ribonuclease III/physiology ; Signal Transduction
Chemical Substances	Hedgehog Proteins ; MicroRNAs ; Patched-1 Receptor ; Protein Isoforms ; Ptch1 protein, mouse ; Dicer1 protein, mouse (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2167-2
ISSN	1943-2631 ; 0016-6731
ISSN (online)	1943-2631
ISSN	0016-6731
DOI	10.1534/genetics.115.184176
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Zs.B 767: Show issues

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Article ; Online: Spatial transcriptomic analysis of Sonic hedgehog medulloblastoma identifies that the loss of heterogeneity and promotion of differentiation underlies the response to CDK4/6 inhibition.

Vo, Tuan / Balderson, Brad / Jones, Kahli / Ni, Guiyan / Crawford, Joanna / Millar, Amanda / Tolson, Elissa / Singleton, Matthew / Kojic, Marija / Robertson, Thomas / Walters, Shaun / Mulay, Onkar / Bhuva, Dharmesh D / Davis, Melissa J / Wainwright, Brandon J / Nguyen, Quan / Genovesi, Laura A

Genome medicine

2023 Volume 15, Issue 1, Page(s) 29

Abstract: Background: Medulloblastoma (MB) is a malignant tumour of the cerebellum which can be classified into four major subgroups based on gene expression and genomic features. Single-cell transcriptome studies have defined the cellular states underlying each ... ...

Abstract	Background: Medulloblastoma (MB) is a malignant tumour of the cerebellum which can be classified into four major subgroups based on gene expression and genomic features. Single-cell transcriptome studies have defined the cellular states underlying each MB subgroup; however, the spatial organisation of these diverse cell states and how this impacts response to therapy remains to be determined. Methods: Here, we used spatially resolved transcriptomics to define the cellular diversity within a sonic hedgehog (SHH) patient-derived model of MB and show that cells specific to a transcriptional state or spatial location are pivotal for CDK4/6 inhibitor, Palbociclib, treatment response. We integrated spatial gene expression with histological annotation and single-cell gene expression data from MB, developing an analysis strategy to spatially map cell type responses within the hybrid system of human and mouse cells and their interface within an intact brain tumour section. Results: We distinguish neoplastic and non-neoplastic cells within tumours and from the surrounding cerebellar tissue, further refining pathological annotation. We identify a regional response to Palbociclib, with reduced proliferation and induced neuronal differentiation in both treated tumours. Additionally, we resolve at a cellular resolution a distinct tumour interface where the tumour contacts neighbouring mouse brain tissue consisting of abundant astrocytes and microglia and continues to proliferate despite Palbociclib treatment. Conclusions: Our data highlight the power of using spatial transcriptomics to characterise the response of a tumour to a targeted therapy and provide further insights into the molecular and cellular basis underlying the response and resistance to CDK4/6 inhibitors in SHH MB.
MeSH term(s)	Animals ; Humans ; Mice ; Cell Differentiation ; Cerebellar Neoplasms/metabolism ; Cyclin-Dependent Kinase 4/genetics ; Cyclin-Dependent Kinase 4/metabolism ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Medulloblastoma/metabolism ; Transcriptome ; Cyclin-Dependent Kinase 6/antagonists & inhibitors
Chemical Substances	CDK4 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Hedgehog Proteins ; Cyclin-Dependent Kinase 6 (EC 2.7.11.22)
Language	English
Publishing date	2023-05-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-023-01185-4
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Article ; Online: Correction: Proliferation of Murine Midbrain Neural Stem Cells Depends upon an Endogenous Sonic Hedgehog (Shh) Source.

Martínez, Constanza / Cornejo, Víctor Hugo / Lois, Pablo / Ellis, Tammy / Solis, Natalia P / Wainwright, Brandon J / Palma, Verónica

PloS one

2020 Volume 15, Issue 9, Page(s) e0239995

Abstract: This corrects the article DOI: 10.1371/journal.pone.0065818.]. ...

Abstract	[This corrects the article DOI: 10.1371/journal.pone.0065818.].
Language	English
Publishing date	2020-09-24
Publishing country	United States
Document type	Published Erratum
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0239995
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