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Article ; Online: HiCRes: a computational method to estimate and predict the genomic resolution of Hi-C libraries.

Marchal, Claire / Singh, Nivedita / Corso-Díaz, Ximena / Swaroop, Anand

2021 Volume 50, Issue 6, Page(s) e35

Abstract: Three-dimensional (3D) conformation of the chromatin is crucial to stringently regulate gene expression patterns and DNA replication in a cell-type specific manner. Hi-C is a key technique for measuring 3D chromatin interactions genome wide. Estimating ... ...

Abstract	Three-dimensional (3D) conformation of the chromatin is crucial to stringently regulate gene expression patterns and DNA replication in a cell-type specific manner. Hi-C is a key technique for measuring 3D chromatin interactions genome wide. Estimating and predicting the resolution of a library is an essential step in any Hi-C experimental design. Here, we present the mathematical concepts to estimate the resolution of a dataset and predict whether deeper sequencing would enhance the resolution. We have developed HiCRes, a docker pipeline, by applying these concepts to several Hi-C libraries.
MeSH term(s)	Chromatin/genetics ; Chromosomes ; Computational Biology/methods ; Gene Library ; Genome ; Genomics
Chemical Substances	Chromatin
Language	English
Publishing date	2021-12-20
Publishing country	England
Document type	Journal Article
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkab1235
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Article ; Online: Aging of the Retina: Molecular and Metabolic Turbulences and Potential Interventions.

Campello, Laura / Singh, Nivedita / Advani, Jayshree / Mondal, Anupam K / Corso-Díaz, Ximena / Swaroop, Anand

Annual review of vision science

2021 Volume 7, Page(s) 633–664

Abstract: Multifaceted and divergent manifestations across tissues and cell types have curtailed advances in deciphering the cellular events that accompany advanced age and contribute to morbidities and mortalities. Increase in human lifespan during the past ... ...

Abstract	Multifaceted and divergent manifestations across tissues and cell types have curtailed advances in deciphering the cellular events that accompany advanced age and contribute to morbidities and mortalities. Increase in human lifespan during the past century has heightened awareness of the need to prevent age-associated frailty of neuronal and sensory systems to allow a healthy and productive life. In this review, we discuss molecular and physiological attributes of aging of the retina, with a goal of understanding age-related impairment of visual function. We highlight the epigenome-metabolism nexus and proteostasis as key contributors to retinal aging and discuss lifestyle changes as potential modulators of retinal function. Finally, we deliberate promising intervention strategies for promoting healthy aging of the retina for improved vision.
MeSH term(s)	Aging/physiology ; Humans ; Retina/physiology ; Vision, Ocular
Language	English
Publishing date	2021-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2805730-2
ISSN	2374-4650 ; 2374-4642
ISSN (online)	2374-4650
ISSN	2374-4642
DOI	10.1146/annurev-vision-100419-114940
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Article ; Online: High-resolution genome topology of human retina uncovers super enhancer-promoter interactions at tissue-specific and multifactorial disease loci.

Marchal, Claire / Singh, Nivedita / Batz, Zachary / Advani, Jayshree / Jaeger, Catherine / Corso-Díaz, Ximena / Swaroop, Anand

Nature communications

2022 Volume 13, Issue 1, Page(s) 5827

Abstract: Chromatin organization and enhancer-promoter contacts establish unique spatiotemporal gene expression patterns in distinct cell types. Non-coding genetic variants can influence cellular phenotypes by modifying higher-order transcriptional hubs and ... ...

Abstract	Chromatin organization and enhancer-promoter contacts establish unique spatiotemporal gene expression patterns in distinct cell types. Non-coding genetic variants can influence cellular phenotypes by modifying higher-order transcriptional hubs and consequently gene expression. To elucidate genomic regulation in human retina, we mapped chromatin contacts at high resolution and integrated with super-enhancers (SEs), histone marks, binding of CTCF and select transcription factors. We show that topologically associated domains (TADs) with central SEs exhibit stronger insulation and augmented contact with retinal genes relative to TADs with edge SEs. Merging genome-wide expression quantitative trait loci (eQTLs) with topology map reveals physical links between 100 eQTLs and corresponding eGenes associated with retinal neurodegeneration. Additionally, we uncover candidate genes for susceptibility variants linked to age-related macular degeneration and glaucoma. Our study of high-resolution genomic architecture of human retina provides insights into genetic control of tissue-specific functions, suggests paradigms for missing heritability, and enables the dissection of common blinding disease phenotypes.
MeSH term(s)	CCCTC-Binding Factor/genetics ; CCCTC-Binding Factor/metabolism ; Chromatin/genetics ; Enhancer Elements, Genetic/genetics ; Humans ; Promoter Regions, Genetic ; Quantitative Trait Loci/genetics ; Retina/metabolism ; Transcription Factors/metabolism
Chemical Substances	CCCTC-Binding Factor ; Chromatin ; Transcription Factors
Language	English
Publishing date	2022-10-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-33427-1
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Article ; Online: QTL mapping of human retina DNA methylation identifies 87 gene-epigenome interactions in age-related macular degeneration.

Advani, Jayshree / Mehta, Puja A / Hamel, Andrew R / Mehrotra, Sudeep / Kiel, Christina / Strunz, Tobias / Corso-Díaz, Ximena / Kwicklis, Madeline / van Asten, Freekje / Ratnapriya, Rinki / Chew, Emily Y / Hernandez, Dena G / Montezuma, Sandra R / Ferrington, Deborah A / Weber, Bernhard H F / Segrè, Ayellet V / Swaroop, Anand

Nature communications

2024 Volume 15, Issue 1, Page(s) 1972

Abstract: DNA methylation provides a crucial epigenetic mark linking genetic variations to environmental influence. We have analyzed array-based DNA methylation profiles of 160 human retinas with co-measured RNA-seq and >8 million genetic variants, uncovering ... ...

Abstract	DNA methylation provides a crucial epigenetic mark linking genetic variations to environmental influence. We have analyzed array-based DNA methylation profiles of 160 human retinas with co-measured RNA-seq and >8 million genetic variants, uncovering sites of genetic regulation in cis (37,453 methylation quantitative trait loci and 12,505 expression quantitative trait loci) and 13,747 DNA methylation loci affecting gene expression, with over one-third specific to the retina. Methylation and expression quantitative trait loci show non-random distribution and enrichment of biological processes related to synapse, mitochondria, and catabolism. Summary data-based Mendelian randomization and colocalization analyses identify 87 target genes where methylation and gene-expression changes likely mediate the genotype effect on age-related macular degeneration. Integrated pathway analysis reveals epigenetic regulation of immune response and metabolism including the glutathione pathway and glycolysis. Our study thus defines key roles of genetic variations driving methylation changes, prioritizes epigenetic control of gene expression, and suggests frameworks for regulation of macular degeneration pathology by genotype-environment interaction in retina.
MeSH term(s)	Humans ; DNA Methylation/genetics ; Epigenesis, Genetic ; Epigenome ; Macular Degeneration/genetics ; Retina
Language	English
Publishing date	2024-03-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-46063-8
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Article ; Online: Epigenetic control of gene regulation during development and disease: A view from the retina.

Corso-Díaz, Ximena / Jaeger, Catherine / Chaitankar, Vijender / Swaroop, Anand

Progress in retinal and eye research

2018 Volume 65, Page(s) 1–27

Abstract: Complex biological processes, such as organogenesis and homeostasis, are stringently regulated by genetic programs that are fine-tuned by epigenetic factors to establish cell fates and/or to respond to the microenvironment. Gene regulatory networks that ... ...

Abstract	Complex biological processes, such as organogenesis and homeostasis, are stringently regulated by genetic programs that are fine-tuned by epigenetic factors to establish cell fates and/or to respond to the microenvironment. Gene regulatory networks that guide cell differentiation and function are modulated and stabilized by modifications to DNA, RNA and proteins. In this review, we focus on two key epigenetic changes - DNA methylation and histone modifications - and discuss their contribution to retinal development, aging and disease, especially in the context of age-related macular degeneration (AMD) and diabetic retinopathy. We highlight less-studied roles of DNA methylation and provide the RNA expression profiles of epigenetic enzymes in human and mouse retina in comparison to other tissues. We also review computational tools and emergent technologies to profile, analyze and integrate epigenetic information. We suggest implementation of editing tools and single-cell technologies to trace and perturb the epigenome for delineating its role in transcriptional regulation. Finally, we present our thoughts on exciting avenues for exploring epigenome in retinal metabolism, disease modeling, and regeneration.
MeSH term(s)	DNA Methylation/physiology ; Epigenesis, Genetic/physiology ; Epigenomics ; Gene Expression Regulation/physiology ; Gene Regulatory Networks/physiology ; Humans ; Macular Degeneration/genetics ; RNA/metabolism ; Retina/embryology ; Retina/physiology
Chemical Substances	RNA (63231-63-0)
Language	English
Publishing date	2018-03-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	1182683-6
ISSN	1873-1635 ; 1350-9462
ISSN (online)	1873-1635
ISSN	1350-9462
DOI	10.1016/j.preteyeres.2018.03.002
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Article: QTL mapping of human retina DNA methylation identifies 87 gene-epigenome interactions in age-related macular degeneration.

Advani, Jayshree / Corso-Diaz, Ximena / Kwicklis, Madeline / van Asten, Freekje / Ratnapriya, Rinki / Mehta, Puja / Hamel, Andrew / Mahrotra, Sudeep / Segrè, Ayellet / Kiel, Christina / Strunz, Tobias / Weber, Bernhard / Chew, Emily / Hernandez, Dena / Montezuma, Sandra / Ferrington, Deborah / Swaroop, Anand

Research square

2023

Abstract: DNA methylation (DNAm) provides a crucial epigenetic mark linking genetic variations to environmental influence. We analyzed array-based DNAm profiles of 160 human retinas with co-measured RNA-seq and > 8 million genetic variants, uncovering sites of ... ...

Abstract	DNA methylation (DNAm) provides a crucial epigenetic mark linking genetic variations to environmental influence. We analyzed array-based DNAm profiles of 160 human retinas with co-measured RNA-seq and > 8 million genetic variants, uncovering sites of genetic regulation in
Language	English
Publishing date	2023-06-16
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3011096/v1
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Article ; Online: Nr2e1 regulates retinal lamination and the development of Müller glia, S-cones, and glycineric amacrine cells during retinogenesis.

Corso-Díaz, Ximena / Simpson, Elizabeth M

Molecular brain

2015 Volume 8, Page(s) 37

Abstract: Background: Nr2e1 is a nuclear receptor crucial for neural stem cell proliferation and maintenance. In the retina, lack of Nr2e1 results in premature neurogenesis, aberrant blood vessel formation and dystrophy. However, the specific role of Nr2e1 in the ...

Abstract	Background: Nr2e1 is a nuclear receptor crucial for neural stem cell proliferation and maintenance. In the retina, lack of Nr2e1 results in premature neurogenesis, aberrant blood vessel formation and dystrophy. However, the specific role of Nr2e1 in the development of different retinal cell types and its cell-autonomous and non-cell autonomous function(s) during eye development are poorly understood. Results: Here, we studied the retinas of P7 and P21 Nr2e1 (frc/frc) mice and Nr2e1 (+/+) ↔ Nr2e1 (frc/frc) chimeras. We hypothesized that Nr2e1 differentially regulates the development of various retinal cell types, and thus the cellular composition of Nr2e1 (frc/frc) retinas does not simply reflect an overrepresentation of cells born early and underrepresentation of cells born later as a consequence of premature neurogenesis. In agreement with our hypothesis, lack of Nr2e1 resulted in increased numbers of glycinergic amacrine cells with no apparent increase in other amacrine sub-types, normal numbers of Müller glia, the last cell-type to be generated, and increased numbers of Nr2e1 (frc/frc) S-cones in chimeras. Furthermore, Nr2e1 (frc/frc) Müller glia were mispositioned in the retina and misexpressed the ganglion cell-specific transcription factor Brn3a. Nr2e1 (frc/frc) retinas also displayed lamination defects including an ectopic neuropil forming an additional inner plexiform layer. In chimeric mice, retinal thickness was rescued by 34 % of wild-type cells and Nr2e1 (frc/frc) dystrophy-related phenotypes were no longer evident. However, the formation of an ectopic neuropil, misexpression of Brn3a in Müller glia, and abnormal cell numbers in the inner and outer nuclear layers at P7 were not rescued by wild-type cells. Conclusions: Together, these results show that Nr2e1, in addition to having a role in preventing premature cell cycle exit, participates in several other developmental processes during retinogenesis including neurite organization in the inner retina and development of glycinergic amacrine cells, S-cones, and Müller glia. Nr2e1 also regulates various aspects of Müller glia differentiation cell-autonomously. However, Nr2e1 does not have a cell-autonomous role in preventing retinal dystrophy. Thus, Nr2e1 regulates processes involved in neurite development and terminal retinal cell differentiation.
MeSH term(s)	Amacrine Cells/cytology ; Amacrine Cells/metabolism ; Animals ; Cell Count ; Chimera ; Ependymoglial Cells/cytology ; Ependymoglial Cells/metabolism ; Female ; Glial Fibrillary Acidic Protein/metabolism ; Glycine/metabolism ; Green Fluorescent Proteins/metabolism ; Male ; Mice, Inbred C57BL ; Models, Biological ; Neurogenesis ; Receptors, Cytoplasmic and Nuclear/metabolism ; Retina/cytology ; Retina/growth & development ; Retina/metabolism ; Retinal Cone Photoreceptor Cells/cytology ; Retinal Cone Photoreceptor Cells/metabolism ; Retinal Vessels/cytology ; Retinal Vessels/metabolism ; Transcription Factor Brn-3A/metabolism ; beta-Galactosidase/metabolism
Chemical Substances	Glial Fibrillary Acidic Protein ; Nr2e1 protein, mouse ; Pou4f1 protein, mouse ; Receptors, Cytoplasmic and Nuclear ; Transcription Factor Brn-3A ; enhanced green fluorescent protein ; Green Fluorescent Proteins (147336-22-9) ; beta-Galactosidase (EC 3.2.1.23) ; Glycine (TE7660XO1C)
Language	English
Publishing date	2015-06-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2436057-0
ISSN	1756-6606 ; 1756-6606
ISSN (online)	1756-6606
ISSN	1756-6606
DOI	10.1186/s13041-015-0126-x
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Article ; Online: Genome-wide Profiling Identifies DNA Methylation Signatures of Aging in Rod Photoreceptors Associated with Alterations in Energy Metabolism.

Corso-Díaz, Ximena / Gentry, James / Rebernick, Ryan / Jaeger, Catherine / Brooks, Matthew J / van Asten, Freekje / Kooragayala, Keshav / Gieser, Linn / Nellissery, Jacob / Covian, Raul / Cogliati, Tiziana / Mondal, Anupam K / Jiang, Ke / Swaroop, Anand

Cell reports

2020 Volume 31, Issue 3, Page(s) 107525

Abstract: Aging-associated functional decline is accompanied by alterations in the epigenome. To explore DNA modifications that could influence visual function with age, we perform whole-genome bisulfite sequencing of purified mouse rod photoreceptors at four ages ...

Abstract	Aging-associated functional decline is accompanied by alterations in the epigenome. To explore DNA modifications that could influence visual function with age, we perform whole-genome bisulfite sequencing of purified mouse rod photoreceptors at four ages and identify 2,054 differentially methylated regions (DMRs). We detect many DMRs during early stages of aging and in rod regulatory regions, and some of these cluster at chromosomal hotspots, especially on chromosome 10, which includes a longevity interactome. Integration of methylome to age-related transcriptome changes, chromatin signatures, and first-order protein-protein interactions uncover an enrichment of DMRs in altered pathways that are associated with rod function, aging, and energy metabolism. In concordance, we detect reduced basal mitochondrial respiration and increased fatty acid dependency with retinal age in ex vivo assays. Our study reveals age-dependent genomic and chromatin features susceptible to DNA methylation changes in rod photoreceptors and identifies a link between DNA methylation and energy metabolism in aging.
MeSH term(s)	Aging/genetics ; Animals ; DNA Methylation/genetics ; Energy Metabolism/genetics ; Genome-Wide Association Study/methods ; Humans ; Male ; Mice ; Retinal Rod Photoreceptor Cells/metabolism
Language	English
Publishing date	2020-04-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.107525
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Article ; Online: nNOS alpha and nNOS beta localization to aggresome-like inclusions is dependent on HSP90 activity.

Corso-Díaz, Ximena / Krukoff, Teresa L

Journal of neurochemistry

2010 Volume 114, Issue 3, Page(s) 864–872

Abstract: Nitric oxide (NO) is a highly reactive gas that participates in many physiological processes including neuroplasticity and neuronal survival. In brain neurons, NO is produced by two variants of neuronal nitric oxide synthase (nNOS), nNOSalpha and ... ...

Abstract	Nitric oxide (NO) is a highly reactive gas that participates in many physiological processes including neuroplasticity and neuronal survival. In brain neurons, NO is produced by two variants of neuronal nitric oxide synthase (nNOS), nNOSalpha and nNOSbeta. The activity of nNOSalpha is tightly regulated at the transcriptional and post-transcriptional levels. Heat shock protein 90 (HSP90) regulates nNOSalpha activity by facilitating heme insertion into the nNOSalpha monomer, resulting in increased NO production. HSP90 also regulates nNOSalpha degradation through the proteasome pathway. Here, we show in vitro that inhibition of HSP90 with geldanamycin increases nNOS mobility and induces formation of aggresome-like inclusions containing both nNOSalpha and nNOSbeta in primary cortical neurons. We also report the formation of endogenous nNOS-containing aggresome-like inclusions in healthy, untreated, mature primary cortical neurons. We propose that nNOS aggregation may be an additional mechanism for regulating nNOS activity, as has been proposed for inducible nitric oxide synthase. These findings reveal a new role for HSP90 in regulating nNOS sub-cellular localization and underscore the complexity of nNOS regulatory mechanisms.
MeSH term(s)	Animals ; Cell Compartmentation/physiology ; Cell Line ; Cells, Cultured ; Cerebral Cortex/metabolism ; Female ; HSP90 Heat-Shock Proteins/metabolism ; HSP90 Heat-Shock Proteins/physiology ; Humans ; Inclusion Bodies/enzymology ; Inclusion Bodies/ultrastructure ; Isoenzymes/metabolism ; Macromolecular Substances/metabolism ; Neurons/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type I/metabolism ; Rats ; Rats, Sprague-Dawley
Chemical Substances	HSP90 Heat-Shock Proteins ; Isoenzymes ; Macromolecular Substances ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type I (EC 1.14.13.39)
Language	English
Publishing date	2010-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2010.06813.x
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Article: nNOSα and nNOSβ localization to aggresome-like inclusions is dependent on HSP90 activity

Corso-Díaz, Ximena / Krukoff, Teresa L

Journal of neurochemistry. 2010 Aug., v. 114, no. 3

2010

Abstract: J. Neurochem. (2010) 114, 864-872. Nitric oxide (NO) is a highly reactive gas that participates in many physiological processes including neuroplasticity and neuronal survival. In brain neurons, NO is produced by two variants of neuronal nitric oxide ... ...

Abstract	J. Neurochem. (2010) 114, 864-872. Nitric oxide (NO) is a highly reactive gas that participates in many physiological processes including neuroplasticity and neuronal survival. In brain neurons, NO is produced by two variants of neuronal nitric oxide synthase (nNOS), nNOSα and nNOSβ. The activity of nNOSα is tightly regulated at the transcriptional and post-transcriptional levels. Heat shock protein 90 (HSP90) regulates nNOSα activity by facilitating heme insertion into the nNOSα monomer, resulting in increased NO production. HSP90 also regulates nNOSα degradation through the proteasome pathway. Here, we show in vitro that inhibition of HSP90 with geldanamycin increases nNOS mobility and induces formation of aggresome-like inclusions containing both nNOSα and nNOSβ in primary cortical neurons. We also report the formation of endogenous nNOS-containing aggresome-like inclusions in healthy, untreated, mature primary cortical neurons. We propose that nNOS aggregation may be an additional mechanism for regulating nNOS activity, as has been proposed for inducible nitric oxide synthase. These findings reveal a new role for HSP90 in regulating nNOS sub-cellular localization and underscore the complexity of nNOS regulatory mechanisms.
Keywords	nitric oxide
Language	English
Dates of publication	2010-08
Size	p. 864-872.
Publisher	Blackwell Publishing Ltd
Publishing place	Oxford, UK
Document type	Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2010.06813.x
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