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...

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Authors: 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
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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spelling 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
url 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
rights_invalid_str_mv cc-by (c) Sirés, Anna et al., 2023
https://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv Articles publicats en revistes (Ciències Fisiològiques)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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