Identification of an evx1-dependent joint-formation pathway during FIN regeneration.

Joints are essential for skeletal flexibly and form, yet the process underlying joint morphogenesis is poorly understood. Zebrafish caudal fins are comprised of numerous segmented bony fin rays, where growth occurs by the sequential addition of new segments and new joints. Here, we evaluate joint ge...

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Main Authors: Quynh V Ton, M Kathryn Iovine
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3835681?pdf=render
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spelling doaj-f12671105e1e441180475fed4cac03c62020-11-25T01:44:58ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-01811e8124010.1371/journal.pone.0081240Identification of an evx1-dependent joint-formation pathway during FIN regeneration.Quynh V TonM Kathryn IovineJoints are essential for skeletal flexibly and form, yet the process underlying joint morphogenesis is poorly understood. Zebrafish caudal fins are comprised of numerous segmented bony fin rays, where growth occurs by the sequential addition of new segments and new joints. Here, we evaluate joint gene expression during fin regeneration. First, we identify three genes that influence joint formation, evx1, dlx5a, and mmp9. We place these genes in a common molecular pathway by evaluating both their expression patterns along the distal-proximal axis (i.e. where the youngest tissue is always the most distal), and by evaluating changes in gene expression following gene knockdown. Prior studies from our lab indicate that the gap junction protein Cx43 suppresses joint formation. Remarkably, changes in Cx43 activity alter the expression of joint markers. For example, the reduced levels of Cx43 in the sof (b123) mutant causes short fin ray segments/premature joints. We also find that the expression of evx1-dlx5a-mmp9 is shifted distally in sof (b123) , consistent with premature expression of these genes. In contrast, increased Cx43 in the alf (dty86) mutant leads to stochastic joint failure and stochastic loss of evx1 expression. Indeed, reducing the level of Cx43 in alf (dty86) rescues both the evx1 expression and joint formation. These results suggest that Cx43 influences the pattern of joint formation by influencing the timing of evx1 expression.http://europepmc.org/articles/PMC3835681?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Quynh V Ton
M Kathryn Iovine
spellingShingle Quynh V Ton
M Kathryn Iovine
Identification of an evx1-dependent joint-formation pathway during FIN regeneration.
PLoS ONE
author_facet Quynh V Ton
M Kathryn Iovine
author_sort Quynh V Ton
title Identification of an evx1-dependent joint-formation pathway during FIN regeneration.
title_short Identification of an evx1-dependent joint-formation pathway during FIN regeneration.
title_full Identification of an evx1-dependent joint-formation pathway during FIN regeneration.
title_fullStr Identification of an evx1-dependent joint-formation pathway during FIN regeneration.
title_full_unstemmed Identification of an evx1-dependent joint-formation pathway during FIN regeneration.
title_sort identification of an evx1-dependent joint-formation pathway during fin regeneration.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2013-01-01
description Joints are essential for skeletal flexibly and form, yet the process underlying joint morphogenesis is poorly understood. Zebrafish caudal fins are comprised of numerous segmented bony fin rays, where growth occurs by the sequential addition of new segments and new joints. Here, we evaluate joint gene expression during fin regeneration. First, we identify three genes that influence joint formation, evx1, dlx5a, and mmp9. We place these genes in a common molecular pathway by evaluating both their expression patterns along the distal-proximal axis (i.e. where the youngest tissue is always the most distal), and by evaluating changes in gene expression following gene knockdown. Prior studies from our lab indicate that the gap junction protein Cx43 suppresses joint formation. Remarkably, changes in Cx43 activity alter the expression of joint markers. For example, the reduced levels of Cx43 in the sof (b123) mutant causes short fin ray segments/premature joints. We also find that the expression of evx1-dlx5a-mmp9 is shifted distally in sof (b123) , consistent with premature expression of these genes. In contrast, increased Cx43 in the alf (dty86) mutant leads to stochastic joint failure and stochastic loss of evx1 expression. Indeed, reducing the level of Cx43 in alf (dty86) rescues both the evx1 expression and joint formation. These results suggest that Cx43 influences the pattern of joint formation by influencing the timing of evx1 expression.
url http://europepmc.org/articles/PMC3835681?pdf=render
work_keys_str_mv AT quynhvton identificationofanevx1dependentjointformationpathwayduringfinregeneration
AT mkathryniovine identificationofanevx1dependentjointformationpathwayduringfinregeneration
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