Thyroid Hormone Signaling in the Mouse Retina.
Thyroid hormone is a crucial regulator of gene expression in the developing and adult retina. Here we sought to map sites of thyroid hormone signaling at the cellular level using the transgenic FINDT3 reporter mouse model in which neurons express β-galactosidase (β-gal) under the control of a hybrid...
Main Authors: | , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2016-01-01
|
Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC5152892?pdf=render |
id |
doaj-1824c1a5431241fd8fef9b84928b3d7d |
---|---|
record_format |
Article |
spelling |
doaj-1824c1a5431241fd8fef9b84928b3d7d2020-11-25T00:08:37ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-011112e016800310.1371/journal.pone.0168003Thyroid Hormone Signaling in the Mouse Retina.Patrick ArbogastFrédéric FlamantPierre GodementMartin GlösmannLeo PeichlThyroid hormone is a crucial regulator of gene expression in the developing and adult retina. Here we sought to map sites of thyroid hormone signaling at the cellular level using the transgenic FINDT3 reporter mouse model in which neurons express β-galactosidase (β-gal) under the control of a hybrid Gal4-TRα receptor when triiodothyronine (T3) and cofactors of thyroid receptor signaling are present. In the adult retina, nearly all neurons of the ganglion cell layer (GCL, ganglion cells and displaced amacrine cells) showed strong β-gal labeling. In the inner nuclear layer (INL), a minority of glycineric and GABAergic amacrine cells showed β-gal labeling, whereas the majority of amacrine cells were unlabeled. At the level of amacrine types, β-gal labeling was found in a large proportion of the glycinergic AII amacrines, but only in a small proportion of the cholinergic/GABAergic 'starburst' amacrines. At postnatal day 10, there also was a high density of strongly β-gal-labeled neurons in the GCL, but only few amacrine cells were labeled in the INL. There was no labeling of bipolar cells, horizontal cells and Müller glia cells at both stages. Most surprisingly, the photoreceptor somata in the outer nuclear layer also showed no β-gal label, although thyroid hormone is known to control cone opsin expression. This is the first record of thyroid hormone signaling in the inner retina of an adult mammal. We hypothesize that T3 levels in photoreceptors are below the detection threshold of the reporter system. The topographical distribution of β-gal-positive cells in the GCL follows the overall neuron distribution in that layer, with more T3-signaling cells in the ventral than the dorsal half-retina.http://europepmc.org/articles/PMC5152892?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Patrick Arbogast Frédéric Flamant Pierre Godement Martin Glösmann Leo Peichl |
spellingShingle |
Patrick Arbogast Frédéric Flamant Pierre Godement Martin Glösmann Leo Peichl Thyroid Hormone Signaling in the Mouse Retina. PLoS ONE |
author_facet |
Patrick Arbogast Frédéric Flamant Pierre Godement Martin Glösmann Leo Peichl |
author_sort |
Patrick Arbogast |
title |
Thyroid Hormone Signaling in the Mouse Retina. |
title_short |
Thyroid Hormone Signaling in the Mouse Retina. |
title_full |
Thyroid Hormone Signaling in the Mouse Retina. |
title_fullStr |
Thyroid Hormone Signaling in the Mouse Retina. |
title_full_unstemmed |
Thyroid Hormone Signaling in the Mouse Retina. |
title_sort |
thyroid hormone signaling in the mouse retina. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2016-01-01 |
description |
Thyroid hormone is a crucial regulator of gene expression in the developing and adult retina. Here we sought to map sites of thyroid hormone signaling at the cellular level using the transgenic FINDT3 reporter mouse model in which neurons express β-galactosidase (β-gal) under the control of a hybrid Gal4-TRα receptor when triiodothyronine (T3) and cofactors of thyroid receptor signaling are present. In the adult retina, nearly all neurons of the ganglion cell layer (GCL, ganglion cells and displaced amacrine cells) showed strong β-gal labeling. In the inner nuclear layer (INL), a minority of glycineric and GABAergic amacrine cells showed β-gal labeling, whereas the majority of amacrine cells were unlabeled. At the level of amacrine types, β-gal labeling was found in a large proportion of the glycinergic AII amacrines, but only in a small proportion of the cholinergic/GABAergic 'starburst' amacrines. At postnatal day 10, there also was a high density of strongly β-gal-labeled neurons in the GCL, but only few amacrine cells were labeled in the INL. There was no labeling of bipolar cells, horizontal cells and Müller glia cells at both stages. Most surprisingly, the photoreceptor somata in the outer nuclear layer also showed no β-gal label, although thyroid hormone is known to control cone opsin expression. This is the first record of thyroid hormone signaling in the inner retina of an adult mammal. We hypothesize that T3 levels in photoreceptors are below the detection threshold of the reporter system. The topographical distribution of β-gal-positive cells in the GCL follows the overall neuron distribution in that layer, with more T3-signaling cells in the ventral than the dorsal half-retina. |
url |
http://europepmc.org/articles/PMC5152892?pdf=render |
work_keys_str_mv |
AT patrickarbogast thyroidhormonesignalinginthemouseretina AT fredericflamant thyroidhormonesignalinginthemouseretina AT pierregodement thyroidhormonesignalinginthemouseretina AT martinglosmann thyroidhormonesignalinginthemouseretina AT leopeichl thyroidhormonesignalinginthemouseretina |
_version_ |
1725415441612931072 |