The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retina
The short and long isoforms of FAIM (FAIM-S and FAIM-L) hold important functions in the central nervous system, and their expression levels are specifically enriched in the retina. We previously described that Faim knockout (KO) mice present structural and molecular alterations in the retina compati...
| Authors: | , , , , , , , , |
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| Format: | article |
| Status: | Published version |
| Publication Date: | 2023 |
| Country: | España |
| Institution: | Universidad de Barcelona |
| Repository: | Dipòsit Digital de la UB |
| OAI Identifier: | oai:diposit.ub.edu:2445/194080 |
| Online Access: | https://hdl.handle.net/2445/194080 |
| Access Level: | Open access |
| Keyword: | Retina Ratolins (Animals de laboratori) Fotoreceptors Mice (Laboratory animals) Photoreceptors |
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The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retinaSirés, AnnaPazo-González, MateoLópez-Soriano, JoaquínMéndez, Anade la Rosa, Enrique J.de la Villa, PedroComella, Joan X.Hernández-Sánchez, CatalinaSolé, MontseRetinaRatolins (Animals de laboratori)FotoreceptorsRetinaMice (Laboratory animals)PhotoreceptorsThe short and long isoforms of FAIM (FAIM-S and FAIM-L) hold important functions in the central nervous system, and their expression levels are specifically enriched in the retina. We previously described that Faim knockout (KO) mice present structural and molecular alterations in the retina compatible with a neurodegenerative phenotype. Here, we aimed to study Faim KO retinal functions and molecular mechanisms leading to its alterations. Electroretinographic recordings showed that aged Faim KO mice present functional loss of rod photoreceptor and ganglion cells. Additionally, we found a significant delay in dark adaptation from early adult ages. This functional deficit is exacerbated by luminic stress, which also caused histopathological alterations. Interestingly, Faim KO mice present abnormal Arrestin-1 redistribution upon light reception, and we show that Arrestin-1 is ubiquitinated, a process that is abrogated by either FAIM-S or FAIM-L in vitro. Our results suggest that FAIM assists Arrestin-1 light-dependent translocation by a process that likely involves ubiquitination. In the absence of FAIM, this impairment could be the cause of dark adaptation delay and increased light sensitivity. Multiple retinal diseases are linked to deficits in photoresponse termination, and hence, investigating the role of FAIM could shed light onto the underlying mechanisms of their pathophysiology.MDPI2023info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/2445/194080Articles publicats en revistes (Ciències Fisiològiques)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésReproducció del document publicat a: https://doi.org/10.3390/cells12030487Cells, 2023, vol. 12, num. 3, p. 487https://doi.org/10.3390/cells12030487cc-by (c) Sirés, Anna et al., 2023https://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1940802026-05-27T06:46:51Z |
| dc.title.none.fl_str_mv |
The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retina |
| title |
The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retina |
| spellingShingle |
The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retina Sirés, Anna Retina Ratolins (Animals de laboratori) Fotoreceptors Retina Mice (Laboratory animals) Photoreceptors |
| title_short |
The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retina |
| title_full |
The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retina |
| title_fullStr |
The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retina |
| title_full_unstemmed |
The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retina |
| title_sort |
The absence of FAIM leads to a delay in dark adaptation and hampers arrestin-1 translocation upon light reception in the retina |
| dc.creator.none.fl_str_mv |
Sirés, Anna Pazo-González, Mateo López-Soriano, Joaquín Méndez, Ana de la Rosa, Enrique J. de la Villa, Pedro Comella, Joan X. Hernández-Sánchez, Catalina Solé, Montse |
| author |
Sirés, Anna |
| author_facet |
Sirés, Anna Pazo-González, Mateo López-Soriano, Joaquín Méndez, Ana de la Rosa, Enrique J. de la Villa, Pedro Comella, Joan X. Hernández-Sánchez, Catalina Solé, Montse |
| author_role |
author |
| author2 |
Pazo-González, Mateo López-Soriano, Joaquín Méndez, Ana de la Rosa, Enrique J. de la Villa, Pedro Comella, Joan X. Hernández-Sánchez, Catalina Solé, Montse |
| author2_role |
author author author author author author author author |
| dc.subject.none.fl_str_mv |
Retina Ratolins (Animals de laboratori) Fotoreceptors Retina Mice (Laboratory animals) Photoreceptors |
| topic |
Retina Ratolins (Animals de laboratori) Fotoreceptors Retina Mice (Laboratory animals) Photoreceptors |
| description |
The short and long isoforms of FAIM (FAIM-S and FAIM-L) hold important functions in the central nervous system, and their expression levels are specifically enriched in the retina. We previously described that Faim knockout (KO) mice present structural and molecular alterations in the retina compatible with a neurodegenerative phenotype. Here, we aimed to study Faim KO retinal functions and molecular mechanisms leading to its alterations. Electroretinographic recordings showed that aged Faim KO mice present functional loss of rod photoreceptor and ganglion cells. Additionally, we found a significant delay in dark adaptation from early adult ages. This functional deficit is exacerbated by luminic stress, which also caused histopathological alterations. Interestingly, Faim KO mice present abnormal Arrestin-1 redistribution upon light reception, and we show that Arrestin-1 is ubiquitinated, a process that is abrogated by either FAIM-S or FAIM-L in vitro. Our results suggest that FAIM assists Arrestin-1 light-dependent translocation by a process that likely involves ubiquitination. In the absence of FAIM, this impairment could be the cause of dark adaptation delay and increased light sensitivity. Multiple retinal diseases are linked to deficits in photoresponse termination, and hence, investigating the role of FAIM could shed light onto the underlying mechanisms of their pathophysiology. |
| publishDate |
2023 |
| dc.date.none.fl_str_mv |
2023 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
| format |
article |
| status_str |
publishedVersion |
| dc.identifier.none.fl_str_mv |
https://hdl.handle.net/2445/194080 |
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https://hdl.handle.net/2445/194080 |
| dc.language.none.fl_str_mv |
Inglés |
| language_invalid_str_mv |
Inglés |
| dc.relation.none.fl_str_mv |
Reproducció del document publicat a: https://doi.org/10.3390/cells12030487 Cells, 2023, vol. 12, num. 3, p. 487 https://doi.org/10.3390/cells12030487 |
| dc.rights.none.fl_str_mv |
cc-by (c) Sirés, Anna et al., 2023 https://creativecommons.org/licenses/by/4.0/ info:eu-repo/semantics/openAccess |
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cc-by (c) Sirés, Anna et al., 2023 https://creativecommons.org/licenses/by/4.0/ |
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openAccess |
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application/pdf |
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MDPI |
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MDPI |
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