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Article ; Online: Chloride intracellular channel (CLIC) proteins function as fusogens.

Manori, Bar / Vaknin, Alisa / Vaňková, Pavla / Nitzan, Anat / Zaidel-Bar, Ronen / Man, Petr / Giladi, Moshe / Haitin, Yoni

Nature communications

2024 Volume 15, Issue 1, Page(s) 2085

Abstract: Chloride Intracellular Channel (CLIC) family members uniquely transition between soluble and membrane-associated conformations. Despite decades of extensive functional and structural studies, CLICs' function as ion channels remains debated, rendering our ...

Abstract	Chloride Intracellular Channel (CLIC) family members uniquely transition between soluble and membrane-associated conformations. Despite decades of extensive functional and structural studies, CLICs' function as ion channels remains debated, rendering our understanding of their physiological role incomplete. Here, we expose the function of CLIC5 as a fusogen. We demonstrate that purified CLIC5 directly interacts with the membrane and induces fusion, as reflected by increased liposomal diameter and lipid and content mixing between liposomes. Moreover, we show that this activity is facilitated by acidic pH, a known trigger for CLICs' transition to a membrane-associated conformation, and that increased exposure of the hydrophobic inter-domain interface is crucial for this process. Finally, mutation of a conserved hydrophobic interfacial residue diminishes the fusogenic activity of CLIC5 in vitro and impairs excretory canal extension in C. elegans in vivo. Together, our results unravel the long-sought physiological role of these enigmatic proteins.
MeSH term(s)	Animals ; Chlorides/metabolism ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Chloride Channels/metabolism ; Liposomes
Chemical Substances	Chlorides ; Chloride Channels ; Liposomes
Language	English
Publishing date	2024-03-07
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/s41467-024-46301-z
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Article ; Online: Actin-capping protein regulates actomyosin contractility to maintain germline architecture in C. elegans.

Ray, Shinjini / Agarwal, Priti / Nitzan, Anat / Nédélec, François / Zaidel-Bar, Ronen

Development (Cambridge, England)

2023 Volume 150, Issue 6

Abstract: Actin dynamics play an important role in tissue morphogenesis, yet the control of actin filament growth takes place at the molecular level. A challenge in the field is to link the molecular function of actin regulators with their physiological function. ... ...

Abstract	Actin dynamics play an important role in tissue morphogenesis, yet the control of actin filament growth takes place at the molecular level. A challenge in the field is to link the molecular function of actin regulators with their physiological function. Here, we report an in vivo role of the actin-capping protein CAP-1 in the Caenorhabditis elegans germline. We show that CAP-1 is associated with actomyosin structures in the cortex and rachis, and its depletion or overexpression led to severe structural defects in the syncytial germline and oocytes. A 60% reduction in the level of CAP-1 caused a twofold increase in F-actin and non-muscle myosin II activity, and laser incision experiments revealed an increase in rachis contractility. Cytosim simulations pointed to increased myosin as the main driver of increased contractility following loss of actin-capping protein. Double depletion of CAP-1 and myosin or Rho kinase demonstrated that the rachis architecture defects associated with CAP-1 depletion require contractility of the rachis actomyosin corset. Thus, we uncovered a physiological role for actin-capping protein in regulating actomyosin contractility to maintain reproductive tissue architecture.
MeSH term(s)	Animals ; Actomyosin/metabolism ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Actins/metabolism ; Actin Capping Proteins/metabolism ; Actin Cytoskeleton/metabolism ; Myosins/metabolism ; Germ Cells/metabolism
Chemical Substances	Actomyosin (9013-26-7) ; Actins ; Actin Capping Proteins ; Myosins (EC 3.6.4.1)
Language	English
Publishing date	2023-03-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.201099
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Article ; Online: Mild carotid stenosis creates gradual, progressive, lifelong brain, and eye damage: An experimental laboratory rat model.

Tzameret, Adi / Piontkewitz, Yael / Nitzan, Anat / Rudoler, Nir / Bruzel, Marina / Zilberstein, Yael / Ziv, Hana / Pri-Chen, Sarah / Solomon, Arieh S

The Journal of comparative neurology

2020 Volume 528, Issue 10, Page(s) 1672–1682

Abstract: In humans, carotid stenosis of 70% and above might be the cause of clinical symptoms such as transient ischemic attack and stroke. No clinical or animal studies have evaluated mild carotid occlusion, and few examined unilateral occlusion. Here, Westar ... ...

Abstract	In humans, carotid stenosis of 70% and above might be the cause of clinical symptoms such as transient ischemic attack and stroke. No clinical or animal studies have evaluated mild carotid occlusion, and few examined unilateral occlusion. Here, Westar rats underwent bilateral or unilateral carotid occlusion of 28-45%. Long-term effects were evaluated 9-11 months later. We conducted cognitive evaluation using spatial learning in a water maze and exploration behavior in an open field. Morphology of the brain was examined by MRI using diffusion-tensor imaging (DTI) and immunohistochemistry staining of the brain and eyes. Cognitive deficit was found in spatial memory and exploration behavior in both occluded groups. Brain and eyes histology presented severe damage in the bilateral group, compared to the unilateral one. DTI revealed an increase in mean diffusivity (MD) in the ventral thalamus and a decrease in fractional anisotropy in optic nerve and optic tract in bilateral rats, while unilateral rats showed only an increase in MD in the ventral pons. In those areas, a significant change in astrocytes, microglia, and number of apoptotic cells were found. Bilateral occlusion produced severe damage to both retinas, while unilateral occlusion produced damage mainly in the occluded side. We found that mild carotid stenosis, even in a unilateral occlusion, creates behavioral abnormalities presented by brain and eye histopathology. The results support our hypothesis that gradual formation of mild carotid stenosis along the life course leads to progressive damage that may create different degenerative diseases at a later age.
MeSH term(s)	Animals ; Brain/pathology ; Carotid Stenosis/complications ; Cognitive Dysfunction/etiology ; Disease Models, Animal ; Eye/pathology ; Male ; Maze Learning ; Optic Nerve/pathology ; Optic Tract/pathology ; Rats ; Rats, Wistar
Language	English
Publishing date	2020-01-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3086-7
ISSN	1096-9861 ; 0021-9967 ; 0092-7317
ISSN (online)	1096-9861
ISSN	0021-9967 ; 0092-7317
DOI	10.1002/cne.24851
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Article ; Online: Levodopa-responsive dystonia caused by biallelic

Mor-Shaked, Hagar / Paz-Ebstein, Emuna / Basal, Adily / Ben-Haim, Simona / Grobe, Hanna / Heymann, Sami / Israel, Zvi / Namnah, Montaser / Nitzan, Anat / Rosenbluh, Chaggai / Saada, Ann / Tzur, Tomer / Yanovsky-Dagan, Shira / Zaidel-Bar, Ronen / Harel, Tamar / Arkadir, David

Brain communications

2021 Volume 3, Issue 3, Page(s) fcab197

Abstract: Biallelic pathogenic variants ... ...

Abstract	Biallelic pathogenic variants in
Language	English
Publishing date	2021-09-06
Publishing country	England
Document type	Journal Article
ISSN	2632-1297
ISSN (online)	2632-1297
DOI	10.1093/braincomms/fcab197
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Article ; Online: Inhibition of Sema-3A Promotes Cell Migration, Axonal Growth, and Retinal Ganglion Cell Survival.

Nitzan, Anat / Corredor-Sanchez, Miriam / Galron, Ronit / Nahary, Limor / Safrin, Mary / Bruzel, Marina / Moure, Alejandra / Bonet, Roman / Pérez, Yolanda / Bujons, Jordi / Vallejo-Yague, Enriqueta / Sacks, Hagit / Burnet, Michael / Alfonso, Ignacio / Messeguer, Angel / Benhar, Itai / Barzilai, Ari / Solomon, Arieh S

Translational vision science & technology

2021 Volume 10, Issue 10, Page(s) 16

Abstract: Purpose: Semaphorin 3A (Sema-3A) is a secreted protein that deflects axons from inappropriate regions and induces neuronal cell death. Intravitreal application of polyclonal antibodies against Sema-3A prevents loss of retinal ganglion cells ensuing from ...

Abstract	Purpose: Semaphorin 3A (Sema-3A) is a secreted protein that deflects axons from inappropriate regions and induces neuronal cell death. Intravitreal application of polyclonal antibodies against Sema-3A prevents loss of retinal ganglion cells ensuing from axotomy of optic nerves. This suggested a therapeutic approach for neuroprotection via inhibition of the Sema-3A pathway. Methods: To develop potent and specific Sema-3A antagonists, we isolated monoclonal anti-Sema-3A antibodies from a human antibody phage display library and optimized low-molecular weight Sema-3A signaling inhibitors. The best inhibitors were identified using in vitro scratch assays and semiquantitative repulsion assays. Results: A therapeutic approach for neuroprotection must have a long duration of action. Therefore, antibodies and low-molecular weight inhibitors were formulated in extruded implants to allow controlled and prolonged release. Following release from the implants, Sema-3A inhibitors antagonized Sema-3A effects in scratch and repulsion assays and protected retinal ganglion cells in animal models of optic nerve injury, retinal ischemia, and glaucoma. Conclusions and translational relevance: Collectively, our findings indicate that the identified Sema-3A inhibitors should be further evaluated as therapeutic candidates for the treatment of Sema-3A-driven central nervous system degenerative processes.
MeSH term(s)	Animals ; Axons ; Axotomy ; Cell Movement ; Humans ; Retinal Ganglion Cells ; Semaphorin-3A
Chemical Substances	Semaphorin-3A
Language	English
Publishing date	2021-11-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2674602-5
ISSN	2164-2591 ; 2164-2591
ISSN (online)	2164-2591
ISSN	2164-2591
DOI	10.1167/tvst.10.10.16
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Article ; Online: Germ Granules Govern Small RNA Inheritance.

Lev, Itamar / Toker, Itai Antoine / Mor, Yael / Nitzan, Anat / Weintraub, Guy / Antonova, Olga / Bhonkar, Ornit / Ben Shushan, Itay / Seroussi, Uri / Claycomb, Julie M / Anava, Sarit / Gingold, Hila / Zaidel-Bar, Ronen / Rechavi, Oded

Current biology : CB

2019 Volume 29, Issue 17, Page(s) 2880–2891.e4

Abstract: In C. elegans nematodes, components of liquid-like germ granules were shown to be required for transgenerational small RNA inheritance. Surprisingly, we show here that mutants with defective germ granules can nevertheless inherit potent small RNA-based ... ...

Abstract	In C. elegans nematodes, components of liquid-like germ granules were shown to be required for transgenerational small RNA inheritance. Surprisingly, we show here that mutants with defective germ granules can nevertheless inherit potent small RNA-based silencing responses, but some of the mutants lose this ability after many generations of homozygosity. Animals mutated in pptr-1, which is required for stabilization of P granules in the early embryo, display extraordinarily strong heritable RNAi responses, lasting for tens of generations. Intriguingly, the RNAi capacity of descendants derived from mutants defective in the core germ granule proteins MEG-3 and MEG-4 is determined by the genotype of the ancestors and changes transgenerationally. Further, whether the meg-3/4 mutant alleles were present in the paternal or maternal lineages leads to different transgenerational consequences. Small RNA inheritance, rather than maternal contribution of the germ granules themselves, mediates the transgenerational defects in RNAi of meg-3/4 mutants and their progeny. Accordingly, germ granule defects lead to heritable genome-wide mis-expression of endogenous small RNAs. Upon disruption of germ granules, hrde-1 mutants can inherit RNAi, although HRDE-1 was previously thought to be absolutely required for RNAi inheritance. We propose that germ granules sort and shape the RNA pool, and that small RNA inheritance maintains this activity for multiple generations.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Germ Cells/metabolism ; Inheritance Patterns ; RNA, Helminth/genetics ; RNA, Small Interfering/genetics
Chemical Substances	RNA, Helminth ; RNA, Small Interfering
Language	English
Publishing date	2019-08-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2019.07.054
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Article ; Online: Upregulation of Semaphorin 3A and the associated biochemical and cellular events in a rat model of retinal detachment.

Klebanov, Olga / Nitzan, Anat / Raz, Dorit / Barzilai, Ari / Solomon, Arieh S

Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie

2009 Volume 247, Issue 1, Page(s) 73–86

Abstract: Background: Retinal detachment, as a result of injury or disease, is a severe disorder that may ultimately lead to complete blindness. Despite advanced surgical repair techniques, the visual acuity of patients is often limited. We investigated some of ... ...

Abstract	Background: Retinal detachment, as a result of injury or disease, is a severe disorder that may ultimately lead to complete blindness. Despite advanced surgical repair techniques, the visual acuity of patients is often limited. We investigated some of the biochemical and morphological alterations following experimental retinal detachment in laboratory animals. Methods: Unilateral retinal detachment was induced in male Wistar rats; contralateral untreated eyes served as a control. Approximately half of the retinal area was detached by a sub-retinal injection of 5 mul Saline. The incidence and extent of the retinal detachment was evaluated using MRI analysis and fundus images. The retinas were collected at intervals of 24 hours, 7, 14 and 28 days following the procedure. Using Western blot and immunohistochemical analysis, the expression levels of Semaphorin3A, Neuropilin1, GAP43 and NF-H were studied. In addition, morphological changes in Müller and microglial cells were examined. TUNEL staining was used to assess apoptosis. Results: We found that the expression level of Semaphorin3A was up-regulated and reached its peak at two time points: 24 hours and 14 days after surgery. A similar pattern of expression was found for Neuropilin1. TUNEL-positive cells, indicating apoptotic processes, were evident 24 hours post retinal detachment and increased after 7 days. On the other hand, GAP43 expression was up-regulated 14 days after retinal detachment, and further intensified 28 days post-surgery. Microglial cells were activated shortly after detachment and concentrated mostly at the inner plexiform layer. GFAP staining revealed hypertrophy of Müller cells. Conclusions: The biochemical and morphological changes suggest that apoptosis as well as axonal regrowth take place following retinal detachment. Collectively, these findings may explain the limited success following repair surgery in terms of visual acuity and physiological function of the retina. Our study may open a new approach for treatment of early phase retinal detachment, as well as improve post-operative care that may, in turn, improve the functional result of the surgery. In addition, further study is required on several other factors that may affect visual acuity, such as size and location of the detached area and the time lapse between detachment and surgery.
MeSH term(s)	Animals ; Apoptosis/physiology ; Axons/physiology ; Blotting, Western ; C-Reactive Protein/metabolism ; Disease Models, Animal ; GAP-43 Protein/metabolism ; Glial Fibrillary Acidic Protein/metabolism ; Immunohistochemistry ; In Situ Nick-End Labeling ; Magnetic Resonance Imaging ; Male ; Microglia/metabolism ; Microglia/pathology ; Nerve Regeneration/physiology ; Nerve Tissue Proteins/metabolism ; Rats ; Rats, Wistar ; Retinal Detachment/metabolism ; Retinal Detachment/pathology ; Retinal Ganglion Cells/metabolism ; Retinal Ganglion Cells/pathology ; Semaphorin-3A/metabolism ; Up-Regulation/physiology
Chemical Substances	GAP-43 Protein ; Glial Fibrillary Acidic Protein ; Nerve Tissue Proteins ; Sema3a protein, rat ; Semaphorin-3A ; neuronal pentraxin ; C-Reactive Protein (9007-41-4)
Language	English
Publishing date	2009-01
Publishing country	Germany
Document type	Journal Article
ZDB-ID	8435-9
ISSN	1435-702X ; 0721-832X
ISSN (online)	1435-702X
ISSN	0721-832X
DOI	10.1007/s00417-008-0945-x
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Article ; Online: Sema-3A indirectly disrupts the regeneration process of goldfish optic nerve after controlled injury.

Rosenzweig, Shira / Raz-Prag, Dorit / Nitzan, Anat / Galron, Ronit / Paz, Ma'ayan / Jeserich, Gunnar / Neufeld, Gera / Barzilai, Ari / Solomon, Arieh S

Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie

2010 Volume 248, Issue 10, Page(s) 1423–1435

Abstract: Background: Neurons of adult mammalian CNS are prevented from regenerating injured axons due to formation of a non-permissive environment. The retinal ganglion cells (RGC), which are part of the CNS, share this characteristic. In sharp contrast, the RGC ...

Abstract	Background: Neurons of adult mammalian CNS are prevented from regenerating injured axons due to formation of a non-permissive environment. The retinal ganglion cells (RGC), which are part of the CNS, share this characteristic. In sharp contrast, the RGC of lower vertebrates, such as fish, are capable of re-growing injured optic nerve axons, and achieve, through a complex multi-factorial process, functional vision after injury. Semaphorin-3A (sema-3A), a member of the class 3 semaphorins known for its repellent and apoptotic activities, has previously been shown to play a key role in the formation of a non-permissive environment after CNS injury in mammalians. Methods: The expression of sema-3A and its effect on regenerative processes in injured gold fish retina and optic nerve were investigated in this study. Unilateral optic nerve axotomy or crush was induced in goldfish. 2 microl sema-3A was injected intraviterally 48 hours post injury. Neuronal viability was measured using the lipophilic neurotracer dye 4-Di-10-Asp. Axonal regeneration was initiated using the anterograde dye dextran. Retinas and optic nerves were collected at intervals of 2, 3, 7, 14 and 28 days after the procedure. Using Western blot and immunohistochemical analysis, the expression levels of semaphorin-3A, axonal regeneration, the removal of myelin debris and macrophage invasion were studied. Results: We found a decrease in sema-3A levels in the retina at an early stage after optic nerve injury, but no change in sema-3A levels in the injured optic nerve. Intravitreal injection of sema-3A to goldfish eye, shortly after optic nerve injury, led to destructive effects on several pathways of the regenerative processes, including the survival of retinal ganglion cells, axonal growth, and clearance of myelin debris from the lesion site by macrophages. Conclusions: Exogenous administration of sema-3A in fish indirectly interferes with the regeneration process of the optic nerve. The findings corroborate our previous findings in mammals, and further validate sema-3A as a key factor in the generation of a non-permissive environment after transection of the optic nerve.
MeSH term(s)	Animals ; Axons/physiology ; Axotomy ; Blotting, Western ; Cell Count ; Cell Survival ; Fluorescent Antibody Technique, Indirect ; Goldfish ; Injections ; Macrophages/physiology ; Nerve Crush ; Nerve Regeneration/drug effects ; Nerve Regeneration/physiology ; Optic Nerve/physiology ; Retinal Ganglion Cells/physiology ; Semaphorin-3A/pharmacology ; Semaphorin-3A/physiology ; Vitreous Body
Chemical Substances	Semaphorin-3A
Language	English
Publishing date	2010-05-07
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	8435-9
ISSN	1435-702X ; 0721-832X
ISSN (online)	1435-702X
ISSN	0721-832X
DOI	10.1007/s00417-010-1377-y
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Article: Examination of cellular and molecular events associated with optic nerve axotomy.

Nitzan, Anat / Kermer, Pawel / Shirvan, Anat / Bähr, Mathias / Barzilai, Ari / Solomon, Arieh S

Glia

2006 Volume 54, Issue 6, Page(s) 545–556

Abstract: Purpose: Analyzing cellular behavior during scar formation and determining the expression of growth inhibiting molecules in the optic nerve and retina following acute optic nerve injury.: Methods: A rat model of complete transection of the optic ... ...

Abstract	Purpose: Analyzing cellular behavior during scar formation and determining the expression of growth inhibiting molecules in the optic nerve and retina following acute optic nerve injury. Methods: A rat model of complete transection of the optic nerve that spares the vascular supply and the neural scaffold was used. The response of the optic nerve and retinas to axotomy was studied by immunological and biochemical approaches. Results: Optic nerve axotomy led to massive cell invasion at the site of injury that spread along both sides of the nerve. The cells were microglia, oligodendrocytes, and to a lesser extent astrocytes. A marked induction of semaphorin 3A was evident, especially in the area of the scar, and persisted up to the 28th day of the experiment. Expression of neuropilin-1, a component of the semaphorin 3A receptor, increased following injury. The molecular events associated with axotomy were studied by measuring the levels of semaphorin 3A, p38 MAPK, and ERK1/2 in the retina. Semaphorin 3A levels and the activated form of p38 were elevated 3 days post-axotomy and then declined; ERK1/2 activation levels reached their peak 14 days post axotomy. Acute nerve injury led to morphological alterations in oligodendrocytes, astrocytes, and the extracellular matrix, disrupting the delicate internal organization of the optic nerve. Conclusions: We suggest that cell invasion, semaphorin 3A and neuropilin-1 induction, and disruption of the internal organization of the optic nerve contribute to axotomy-induced degenerative processes.
MeSH term(s)	Animals ; Axons/metabolism ; Axons/pathology ; Axotomy ; Cell Movement/physiology ; Disease Models, Animal ; Disease Progression ; Gliosis/etiology ; Gliosis/metabolism ; Gliosis/physiopathology ; Male ; Microglia/cytology ; Microglia/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Nerve Regeneration/physiology ; Neuropilin-1/metabolism ; Oligodendroglia/cytology ; Oligodendroglia/metabolism ; Optic Nerve/metabolism ; Optic Nerve/pathology ; Optic Nerve/physiopathology ; Optic Nerve Injuries/metabolism ; Optic Nerve Injuries/physiopathology ; Rats ; Rats, Wistar ; Semaphorin-3A/metabolism ; Wallerian Degeneration/etiology ; Wallerian Degeneration/metabolism ; Wallerian Degeneration/physiopathology
Chemical Substances	Sema3a protein, rat ; Semaphorin-3A ; Neuropilin-1 (144713-63-3) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24)
Language	English
Publishing date	2006-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.20398
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Article ; Online: Conditional inactivation of the NBS1 gene in the mouse central nervous system leads to neurodegeneration and disorganization of the visual system.

Baranes, Koby / Raz-Prag, Dorit / Nitzan, Anat / Galron, Ronit / Ashery-Padan, Ruth / Rotenstreich, Ygal / Assaf, Yaniv / Shiloh, Yosef / Wang, Zhao-Qi / Barzilai, Ari / Solomon, Arieh S

Experimental neurology

2009 Volume 218, Issue 1, Page(s) 24–32

Abstract: Nijmegen breakage syndrome (NBS) is a genomic instability disease caused by hypomorphic mutations in the NBS1 gene encoding the Nbs1 (nibrin) protein. Nbs1 is a component of the Mre11/Rad50/Nbs1 (MRN) complex that acts as a sensor of double strand breaks ...

Abstract	Nijmegen breakage syndrome (NBS) is a genomic instability disease caused by hypomorphic mutations in the NBS1 gene encoding the Nbs1 (nibrin) protein. Nbs1 is a component of the Mre11/Rad50/Nbs1 (MRN) complex that acts as a sensor of double strand breaks (DSBs) in the DNA and is critical for proper activation of the broad cellular response to DSBs. Conditional disruption of the murine ortholog of the human NBS1, Nbs1, in the CNS of mice was previously reported to cause microcephaly, severe cerebellar atrophy and ataxia. Here we report that conditional targeted disruption of the murine NBS1 gene in the CNS results in mal-development, degeneration, disorganization and dysfunction of the murine visual system, especially in the optic nerve. Nbs1 deletion resulted in reduced diameters of Nbs1-CNS-Delta eye and optic nerve. MRI analysis revealed defective white matter development and organization. Nbs1 inactivation altered the morphology and organization of the glial cells. Interestingly, at the age of two-month-old the levels of the axonal guidance molecule semaphorin-3A and its receptor neuropilin-1 were up-regulated in the retina of the mutant mice, a typical injury response. Electroretinogram analysis revealed marked reduction in a- and b-waves, indicative of decreased retinal function. Our study points to a novel role for Nbs1 in the development, organization and function of the visual system.
MeSH term(s)	Animals ; Cell Cycle Proteins/genetics ; Electroretinography/methods ; Gene Expression Regulation/genetics ; Magnetic Resonance Imaging ; Male ; Mice ; Mice, Transgenic ; Microscopy, Electron/methods ; Mutation/genetics ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/pathology ; Neuroglia/metabolism ; Nuclear Proteins/genetics ; Optic Nerve/pathology ; Optic Nerve/ultrastructure ; Quinolinium Compounds/metabolism ; Retina/pathology ; Retinal Ganglion Cells/metabolism ; Retinal Ganglion Cells/pathology ; Retinal Ganglion Cells/ultrastructure ; Semaphorin-3A/genetics ; Semaphorin-3A/metabolism ; Visual Pathways/abnormalities ; Visual Pathways/physiopathology ; alpha-Defensins/metabolism
Chemical Substances	4-(4-(dihexadecylamino)styryl)-N-methylquinolinium iodide ; Cell Cycle Proteins ; Nijmegen breakage syndrome 1 protein, mouse ; Nuclear Proteins ; Quinolinium Compounds ; Sema3a protein, mouse ; Semaphorin-3A ; alpha-Defensins
Language	English
Publishing date	2009-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2009.03.026
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