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Article ; Online: Epithelial mechanics are maintained by inhibiting cell fusion with age in Drosophila.

Dehn, Ari S / Duhaime, Levi / Gogna, Navdeep / Nishina, Patsy M / Kelley, Kristina / Losick, Vicki P

2023 Volume 136, Issue 20

Abstract: A characteristic of normal aging and age-related diseases is the remodeling of the cellular organization of a tissue through polyploid cell growth. Polyploidy arises from an increase in nuclear ploidy or the number of nuclei per cell. However, it is not ... ...

Abstract	A characteristic of normal aging and age-related diseases is the remodeling of the cellular organization of a tissue through polyploid cell growth. Polyploidy arises from an increase in nuclear ploidy or the number of nuclei per cell. However, it is not known whether age-induced polyploidy is an adaption to stressors or a precursor to degeneration. Here, we find that abdominal epithelium of the adult fruit fly becomes polyploid with age through generation of multinucleated cells by cell fusion. Inhibition of fusion does not improve the lifespan of the fly, but does enhance its biomechanical fitness, a measure of the healthspan of the animal. Remarkably, Drosophila can maintain their epithelial tension and abdominal movements with age when cell fusion is inhibited. Epithelial cell fusion also appears to be dependent on a mechanical cue, as knockdown of Rho kinase, E-cadherin or α-catenin is sufficient to induce multinucleation in young animals. Interestingly, mutations in α-catenin in mice result in retina pigment epithelial multinucleation associated with macular disease. Therefore, we have discovered that polyploid cells arise by cell fusion and contribute to the decline in the biomechanical fitness of the animal with age.
MeSH term(s)	Animals ; Mice ; Drosophila/genetics ; alpha Catenin ; Cell Fusion ; Drosophila Proteins/genetics ; Polyploidy
Chemical Substances	alpha Catenin ; Drosophila Proteins
Language	English
Publishing date	2023-10-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.260974
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Article: Current Views on Chr10q26 Contribution to Age-Related Macular Degeneration.

Gogna, Navdeep / Hyde, Lillian F / Collin, Gayle B / Stone, Lisa / Naggert, Jurgen K / Nishina, Patsy M

Advances in experimental medicine and biology

2023 Volume 1415, Page(s) 27–36

Abstract: Age-related macular degeneration (AMD) is the leading cause of blindness in the global aging population. Familial aggregation and genome-wide association (GWA) studies have identified gene variants associated with AMD, implying a strong genetic ... ...

Abstract	Age-related macular degeneration (AMD) is the leading cause of blindness in the global aging population. Familial aggregation and genome-wide association (GWA) studies have identified gene variants associated with AMD, implying a strong genetic contribution to AMD development. Two loci, on human Chr 1q31 and 10q26, respectively, represent the most influential of all genetic factors. While the role of CFH at Chr 1q31 is well established, uncertainty remains about the genes ARMS2 and HTRA1, at the Chr 10q26 locus. Since both genes are in strong linkage disequilibrium, assigning individual gene effects is difficult. In this chapter, we review current literature about ARMS2 and HTRA1 and their relevance to AMD risk. Future studies will be necessary to unravel the mechanisms by which they contribute to AMD.
MeSH term(s)	Humans ; Aged ; Proteins/genetics ; Serine Endopeptidases/genetics ; Genome-Wide Association Study ; High-Temperature Requirement A Serine Peptidase 1/genetics ; Macular Degeneration/genetics ; Linkage Disequilibrium ; Polymorphism, Single Nucleotide ; Complement Factor H/genetics ; Genotype
Chemical Substances	Proteins ; Serine Endopeptidases (EC 3.4.21.-) ; High-Temperature Requirement A Serine Peptidase 1 (EC 3.4.21.-) ; Complement Factor H (80295-65-4)
Language	English
Publishing date	2023-07-13
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	410187-X
ISSN	0065-2598
ISSN	0065-2598
DOI	10.1007/978-3-031-27681-1_5
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Article: The Impact of Adherens and Tight Junctions on Physiological Function and Pathological Changes in the Retina.

Kong, Yang / Naggert, Jürgen K / Nishina, Patsy M

Advances in experimental medicine and biology

2018 Volume 1074, Page(s) 545–551

Abstract: The formation of solid tissues is not a simple aggregation of individual cells but rather an ordered assembly of cells connected by junctions. These junctions provide a diffusion barrier as well as mechanical support and a conduit for signalling changes ... ...

Abstract	The formation of solid tissues is not a simple aggregation of individual cells but rather an ordered assembly of cells connected by junctions. These junctions provide a diffusion barrier as well as mechanical support and a conduit for signalling changes in the environment to the cells. Cell junctions are functionally categorized as occluding (e.g. tight junctions, TJs), anchoring (e.g. adherens junctions, AJs) and communicating junctions (e.g. gap junctions). Each type of the cell junction is formed by protein complexes with extracellular domains and/or intracellular domains, which bind partners that provide scaffolding and signalling components. Cell junctions are ubiquitously expressed in multiple tissues and organs, including the retina. In the retina, their biological impact is not limited to regulating tissue growth and development. Disruption of the complexes mediates both congenital and postnatal pathogenesis. In this review, we will focus on cell junctions, specifically AJs and TJs in the external limiting membrane, in order to articulate their influence on pathophysiology of the retina.
MeSH term(s)	Adherens Junctions/physiology ; Adherens Junctions/ultrastructure ; Cell Communication ; Eye Proteins/genetics ; Eye Proteins/physiology ; Gap Junctions/physiology ; Humans ; Membrane Proteins/deficiency ; Membrane Proteins/genetics ; Membrane Proteins/physiology ; Nerve Tissue Proteins/deficiency ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/physiology ; Retina/physiology ; Retina/physiopathology ; Retina/ultrastructure ; Retinal Diseases/diagnosis ; Retinal Diseases/pathology ; Retinal Diseases/physiopathology ; Retinal Diseases/therapy ; Tight Junctions/physiology ; Tomography, Optical Coherence
Chemical Substances	CRB1 protein, human ; Crb1 protein, mouse ; Eye Proteins ; Membrane Proteins ; Nerve Tissue Proteins
Language	English
Publishing date	2018-05-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-319-75402-4_66
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Article ; Online: Single-Cell RNA Sequencing Reveals Molecular Features of Heterogeneity in the Murine Retinal Pigment Epithelium.

Pandey, Ravi S / Krebs, Mark P / Bolisetty, Mohan T / Charette, Jeremy R / Naggert, Jürgen K / Robson, Paul / Nishina, Patsy M / Carter, Gregory W

International journal of molecular sciences

2022 Volume 23, Issue 18

Abstract: Transcriptomic analysis of the mammalian retinal pigment epithelium (RPE) aims to identify cellular networks that influence ocular development, maintenance, function, and disease. However, available evidence points to RPE cell heterogeneity within native ...

Abstract	Transcriptomic analysis of the mammalian retinal pigment epithelium (RPE) aims to identify cellular networks that influence ocular development, maintenance, function, and disease. However, available evidence points to RPE cell heterogeneity within native tissue, which adds complexity to global transcriptomic analysis. Here, to assess cell heterogeneity, we performed single-cell RNA sequencing of RPE cells from two young adult male C57BL/6J mice. Following quality control to ensure robust transcript identification limited to cell singlets, we detected 13,858 transcripts among 2667 and 2846 RPE cells. Dimensional reduction by principal component analysis and uniform manifold approximation and projection revealed six distinct cell populations. All clusters expressed transcripts typical of RPE cells; the smallest (C1, containing 1-2% of total cells) exhibited the hallmarks of stem and/or progenitor (SP) cells. Placing C1-6 along a pseudotime axis suggested a relative decrease in melanogenesis and SP gene expression and a corresponding increase in visual cycle gene expression upon RPE maturation. K-means clustering of all detected transcripts identified additional expression patterns that may advance the understanding of RPE SP cell maintenance and the evolution of cellular metabolic networks during development. This work provides new insights into the transcriptome of the mouse RPE and a baseline for identifying experimentally induced transcriptional changes in future studies of this tissue.
MeSH term(s)	Animals ; Gene Expression Profiling/methods ; Male ; Mammals ; Mice ; Mice, Inbred C57BL ; Retinal Pigment Epithelium/metabolism ; Sequence Analysis, RNA ; Transcriptome
Language	English
Publishing date	2022-09-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231810419
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Article ; Online: Deficiency in Lyst function leads to accumulation of secreted proteases and reduced retinal adhesion.

Ji, Xiaojie / Zhao, Lihong / Umapathy, Ankita / Fitzmaurice, Bernard / Wang, Jieping / Williams, David S / Chang, Bo / Naggert, Jürgen K / Nishina, Patsy M

PloS one

2022 Volume 17, Issue 3, Page(s) e0254469

Abstract: Chediak-Higashi syndrome, caused by mutations in the Lysosome Trafficking Regulator (Lyst) gene, is a recessive hypopigmentation disorder characterized by albinism, neuropathies, neurodegeneration, and defective immune responses, with enlargement of ... ...

Abstract	Chediak-Higashi syndrome, caused by mutations in the Lysosome Trafficking Regulator (Lyst) gene, is a recessive hypopigmentation disorder characterized by albinism, neuropathies, neurodegeneration, and defective immune responses, with enlargement of lysosomes and lysosome-related organelles. Although recent studies have suggested that Lyst mutations impair the regulation of sizes of lysosome and lysosome-related organelle, the underlying pathogenic mechanism of Chediak-Higashi syndrome is still unclear. Here we show striking evidence that deficiency in LYST protein function leads to accumulation of photoreceptor outer segment phagosomes in retinal pigment epithelial cells, and reduces adhesion between photoreceptor outer segment and retinal pigment epithelial cells in a mouse model of Chediak-Higashi syndrome. In addition, we observe elevated levels of cathepsins, matrix metallopeptidase (MMP) 3 and oxidative stress markers in the retinal pigment epithelium of Lyst mutants. Previous reports showed that impaired degradation of photoreceptor outer segment phagosomes causes elevated oxidative stress, which could consequently lead to increases of cysteine cathepsins and MMPs in the extracellular matrix. Taken together, we conclude that the loss of LYST function causes accumulation of phagosomes in the retinal pigment epithelium and elevation of several extracellular matrix-remodeling proteases through oxidative stress, which may, in turn, reduce retinal adhesion. Our work reveals previously unreported pathogenic events in the retinal pigment epithelium caused by Lyst deficiency. The same pathogenic events may be conserved in other professional phagocytic cells, such as macrophages in the immune system, contributing to overall Chediak-Higashi syndrome pathology.
MeSH term(s)	Peptide Hydrolases
Chemical Substances	Peptide Hydrolases (EC 3.4.-)
Language	English
Publishing date	2022-03-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0254469
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Article ; Online: Genetic Interaction between

Gogna, Navdeep / Weatherly, Sonia / Zhao, Fuxin / Collin, Gayle B / Pinkney, Jai / Stone, Lisa / Naggert, Jürgen K / Carter, Gregory W / Nishina, Patsy M

International journal of molecular sciences

2022 Volume 23, Issue 3

Abstract: ... ...

Abstract	Adipor1
MeSH term(s)	Animals ; Breeding ; Disease Models, Animal ; Epistasis, Genetic ; Eye Proteins/genetics ; Eye Proteins/metabolism ; Homozygote ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mutation ; Ophthalmoscopy ; Phenotype ; Receptors, Adiponectin/genetics ; Receptors, Adiponectin/metabolism ; Retinal Degeneration/genetics ; Retinal Degeneration/metabolism ; Retinal Degeneration/pathology
Chemical Substances	Eye Proteins ; Membrane Proteins ; Mfrp protein, mouse ; Receptors, Adiponectin ; adiponectin receptor 1, mouse
Language	English
Publishing date	2022-01-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23031615
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Article ; Online: A

Hyde, Lillian F / Kong, Yang / Zhao, Lihong / Rao, Sriganesh Ramachandra / Wang, Jieping / Stone, Lisa / Njaa, Andrew / Collin, Gayle B / Krebs, Mark P / Chang, Bo / Fliesler, Steven J / Nishina, Patsy M / Naggert, Jürgen K

International journal of molecular sciences

2022 Volume 23, Issue 19

Abstract: Congenital disorders of glycosylation (CDG) are a heterogenous group of primarily autosomal recessive mendelian diseases caused by disruptions in the synthesis of lipid-linked oligosaccharides and their transfer to proteins. CDGs usually affect multiple ... ...

Abstract	Congenital disorders of glycosylation (CDG) are a heterogenous group of primarily autosomal recessive mendelian diseases caused by disruptions in the synthesis of lipid-linked oligosaccharides and their transfer to proteins. CDGs usually affect multiple organ systems and vary in presentation, even within families. There is currently no cure, and treatment is aimed at ameliorating symptoms and improving quality of life. Here, we describe a chemically induced mouse mutant,
MeSH term(s)	Acetylglucosamine ; Animals ; Aspartic Acid/genetics ; Congenital Disorders of Glycosylation/genetics ; Glycine/genetics ; Humans ; Mice ; Muscle Weakness ; Mutation ; Mutation, Missense ; Phosphates ; Quality of Life ; Retinal Diseases ; Uridine Diphosphate
Chemical Substances	Phosphates ; Aspartic Acid (30KYC7MIAI) ; Uridine Diphosphate (58-98-0) ; Glycine (TE7660XO1C) ; Acetylglucosamine (V956696549)
Language	English
Publishing date	2022-10-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231912005
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Article ; Online: A Splicing Mutation in

Collin, Gayle B / Shi, Lanying / Yu, Minzhong / Akturk, Nurten / Charette, Jeremy R / Hyde, Lillian F / Weatherly, Sonia M / Pera, Martin F / Naggert, Jürgen K / Peachey, Neal S / Nishina, Patsy M / Krebs, Mark P

International journal of molecular sciences

2022 Volume 23, Issue 4

Abstract: Fluid and solute transporters of the retinal pigment epithelium (RPE) are core components of the outer blood-retinal barrier. Characterizing these transporters and their role in retinal homeostasis may provide insights into ocular function and disease. ... ...

Abstract	Fluid and solute transporters of the retinal pigment epithelium (RPE) are core components of the outer blood-retinal barrier. Characterizing these transporters and their role in retinal homeostasis may provide insights into ocular function and disease. Here, we describe RPE defects in
MeSH term(s)	Animals ; Cells, Cultured ; Disease Models, Animal ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mutation/genetics ; RNA Splicing/genetics ; Retina/pathology ; Retinal Detachment/genetics ; Retinal Detachment/pathology ; Retinal Pigment Epithelium/pathology ; Sodium-Bicarbonate Symporters/genetics ; Tomography, Optical Coherence/methods
Chemical Substances	SLC4A5 protein, mouse ; Sodium-Bicarbonate Symporters
Language	English
Publishing date	2022-02-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23042220
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Article ; Online: Identification of Arhgef12 and Prkci as genetic modifiers of retinal dysplasia in the Crb1rd8 mouse model.

Weatherly, Sonia M / Collin, Gayle B / Charette, Jeremy R / Stone, Lisa / Damkham, Nattaya / Hyde, Lillian F / Peterson, James G / Hicks, Wanda / Carter, Gregory W / Naggert, Jürgen K / Krebs, Mark P / Nishina, Patsy M

PLoS genetics

2022 Volume 18, Issue 6, Page(s) e1009798

Abstract: Mutations in the apicobasal polarity gene CRB1 lead to diverse retinal diseases, such as Leber congenital amaurosis, cone-rod dystrophy, retinitis pigmentosa (with and without Coats-like vasculopathy), foveal retinoschisis, macular dystrophy, and ... ...

Abstract	Mutations in the apicobasal polarity gene CRB1 lead to diverse retinal diseases, such as Leber congenital amaurosis, cone-rod dystrophy, retinitis pigmentosa (with and without Coats-like vasculopathy), foveal retinoschisis, macular dystrophy, and pigmented paravenous chorioretinal atrophy. Limited correlation between disease phenotypes and CRB1 alleles, and evidence that patients sharing the same alleles often present with different disease features, suggest that genetic modifiers contribute to clinical variation. Similarly, the retinal phenotype of mice bearing the Crb1 retinal degeneration 8 (rd8) allele varies with genetic background. Here, we initiated a sensitized chemical mutagenesis screen in B6.Cg-Crb1rd8/Pjn, a strain with a mild clinical presentation, to identify genetic modifiers that cause a more severe disease phenotype. Two models from this screen, Tvrm266 and Tvrm323, exhibited increased retinal dysplasia. Genetic mapping with high-throughput exome and candidate-gene sequencing identified causative mutations in Arhgef12 and Prkci, respectively. Epistasis analysis of both strains indicated that the increased dysplastic phenotype required homozygosity of the Crb1rd8 allele. Retinal dysplastic lesions in Tvrm266 mice were smaller and caused less photoreceptor degeneration than those in Tvrm323 mice, which developed an early, large diffuse lesion phenotype. At one month of age, Müller glia and microglia mislocalization at dysplastic lesions in both modifier strains was similar to that in B6.Cg-Crb1rd8/Pjn mice but photoreceptor cell mislocalization was more extensive. External limiting membrane disruption was comparable in Tvrm266 and B6.Cg-Crb1rd8/Pjn mice but milder in Tvrm323 mice. Immunohistological analysis of mice at postnatal day 0 indicated a normal distribution of mitotic cells in Tvrm266 and Tvrm323 mice, suggesting normal early development. Aberrant electroretinography responses were observed in both models but functional decline was significant only in Tvrm323 mice. These results identify Arhgef12 and Prkci as modifier genes that differentially shape Crb1-associated retinal disease, which may be relevant to understanding clinical variability and underlying disease mechanisms in humans.
MeSH term(s)	Animals ; Disease Models, Animal ; Eye Proteins/genetics ; Eye Proteins/metabolism ; Isoenzymes/genetics ; Isoenzymes/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Retina/metabolism ; Retinal Degeneration/genetics ; Retinal Degeneration/metabolism ; Retinal Degeneration/pathology ; Retinal Dysplasia/genetics ; Retinal Dysplasia/metabolism ; Retinal Dysplasia/pathology ; Rho Guanine Nucleotide Exchange Factors/genetics ; Rho Guanine Nucleotide Exchange Factors/metabolism
Chemical Substances	Arhgef12 protein, mouse ; Crb1 protein, mouse ; Eye Proteins ; Isoenzymes ; Membrane Proteins ; Nerve Tissue Proteins ; Rho Guanine Nucleotide Exchange Factors ; Protein Kinase C (EC 2.7.11.13) ; protein kinase C lambda (EC 2.7.11.13)
Language	English
Publishing date	2022-06-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1009798
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Article: Lysosomal Trafficking Regulator (LYST).

Ji, Xiaojie / Chang, Bo / Naggert, Jürgen K / Nishina, Patsy M

Advances in experimental medicine and biology

2016 Volume 854, Page(s) 745–750

Abstract: Regulation of vesicle trafficking to lysosomes and lysosome-related organelles (LROs) as well as regulation of the size of these organelles are critical to maintain their functions. Disruption of the lysosomal trafficking regulator (LYST) results in ... ...

Abstract	Regulation of vesicle trafficking to lysosomes and lysosome-related organelles (LROs) as well as regulation of the size of these organelles are critical to maintain their functions. Disruption of the lysosomal trafficking regulator (LYST) results in Chediak-Higashi syndrome (CHS), a rare autosomal recessive disorder characterized by oculocutaneous albinism, prolonged bleeding, severe immunodeficiency, recurrent bacterial infection, neurologic dysfunction and hemophagocytic lympohistiocytosis (HLH). The classic diagnostic feature of the syndrome is enlarged LROs in all cell types, including lysosomes, melanosomes, cytolytic granules and platelet dense bodies. The most striking CHS ocular pathology observed is an enlargement of melanosomes in the retinal pigment epithelium (RPE), which leads to aberrant distribution of eye pigmentation, and results in photophobia and decreased visual acuity. Understanding the molecular function of LYST and identification of its interacting partners may provide therapeutic targets for CHS and other diseases associated with the regulation of LRO size and/or vesicle trafficking, such as asthma, urticaria and Leishmania amazonensis infections.
MeSH term(s)	Animals ; Chediak-Higashi Syndrome/metabolism ; Chediak-Higashi Syndrome/physiopathology ; Cytoplasmic Granules/metabolism ; Humans ; Lysosomes/metabolism ; Melanosomes/metabolism ; Organelles/metabolism ; Photophobia/metabolism ; Photophobia/physiopathology ; Retinal Pigment Epithelium/metabolism ; Retinal Pigment Epithelium/physiopathology ; Vesicular Transport Proteins/metabolism ; Visual Acuity
Chemical Substances	Vesicular Transport Proteins
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-319-17121-0_99
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