On the evolutionary relationship between chondrocytes and osteoblasts

Vertebrates are the only animals that produce bone, but the molecular genetic basis for this evolutionary novelty remains obscure. Here, we synthesize information from traditional evolutionary and modern molecular genetic studies in order to generate a working hypothesis on the evolution of the gene...

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Main Authors: Patsy eGomez-Picos, B Frank eEames
Format: Article
Language:English
Published: Frontiers Media S.A. 2015-09-01
Series:Frontiers in Genetics
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fgene.2015.00297/full
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author Patsy eGomez-Picos
B Frank eEames
author_facet Patsy eGomez-Picos
B Frank eEames
author_sort Patsy eGomez-Picos
collection DOAJ
description Vertebrates are the only animals that produce bone, but the molecular genetic basis for this evolutionary novelty remains obscure. Here, we synthesize information from traditional evolutionary and modern molecular genetic studies in order to generate a working hypothesis on the evolution of the gene regulatory network (GRN) underlying bone formation. To make this argument, we focus on three skeletal tissues that comprise the majority of the vertebrate skeleton: immature cartilage, mature cartilage, and bone. Immature cartilage is produced during early stages of cartilage differentiation and can persist into adulthood, whereas mature cartilage undergoes additional stages of differentiation, including hypertrophy and mineralization. Functionally, histologically, and embryologically, these three skeletal tissues are very similar, yet unique, suggesting that one might have evolved from another. Traditional studies of the fossil record, comparative anatomy and embryology demonstrate clearly that immature cartilage evolved before mature cartilage or bone. Modern molecular approaches show that the GRNs regulating differentiation of these three skeletal cell fates are similar, yet unique, just like the functional and histological features of the tissues themselves. Intriguingly, the Sox9 GRN driving cartilage formation appears to be dominant to the Runx2 GRN of bone. Emphasizing an embryological and evolutionary transcriptomic view, we hypothesize that the Runx2 GRN underlying bone formation was co-opted from mature cartilage. We discuss how modern molecular genetic experiments, such as comparative transcriptomics, can test this hypothesis directly, meanwhile permitting levels of constraint and adaptation to be evaluated quantitatively. Therefore, comparative transcriptomics may revolutionize understanding of not only the clade-specific evolution of skeletal cells, but also the generation of evolutionary novelties, providing a modern paradigm for the evolutionary process.
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spelling doaj.art-cc4ecc4982e74d0c960c5ef282c5f55d2022-12-22T02:20:06ZengFrontiers Media S.A.Frontiers in Genetics1664-80212015-09-01610.3389/fgene.2015.00297158968On the evolutionary relationship between chondrocytes and osteoblastsPatsy eGomez-Picos0B Frank eEames1University of SaskatchewanUniversity of SaskatchewanVertebrates are the only animals that produce bone, but the molecular genetic basis for this evolutionary novelty remains obscure. Here, we synthesize information from traditional evolutionary and modern molecular genetic studies in order to generate a working hypothesis on the evolution of the gene regulatory network (GRN) underlying bone formation. To make this argument, we focus on three skeletal tissues that comprise the majority of the vertebrate skeleton: immature cartilage, mature cartilage, and bone. Immature cartilage is produced during early stages of cartilage differentiation and can persist into adulthood, whereas mature cartilage undergoes additional stages of differentiation, including hypertrophy and mineralization. Functionally, histologically, and embryologically, these three skeletal tissues are very similar, yet unique, suggesting that one might have evolved from another. Traditional studies of the fossil record, comparative anatomy and embryology demonstrate clearly that immature cartilage evolved before mature cartilage or bone. Modern molecular approaches show that the GRNs regulating differentiation of these three skeletal cell fates are similar, yet unique, just like the functional and histological features of the tissues themselves. Intriguingly, the Sox9 GRN driving cartilage formation appears to be dominant to the Runx2 GRN of bone. Emphasizing an embryological and evolutionary transcriptomic view, we hypothesize that the Runx2 GRN underlying bone formation was co-opted from mature cartilage. We discuss how modern molecular genetic experiments, such as comparative transcriptomics, can test this hypothesis directly, meanwhile permitting levels of constraint and adaptation to be evaluated quantitatively. Therefore, comparative transcriptomics may revolutionize understanding of not only the clade-specific evolution of skeletal cells, but also the generation of evolutionary novelties, providing a modern paradigm for the evolutionary process.http://journal.frontiersin.org/Journal/10.3389/fgene.2015.00297/fullBone and BonesCartilageSOX9 Transcription FactorEvo-Devochondrocytecomparative transcriptomics
spellingShingle Patsy eGomez-Picos
B Frank eEames
On the evolutionary relationship between chondrocytes and osteoblasts
Frontiers in Genetics
Bone and Bones
Cartilage
SOX9 Transcription Factor
Evo-Devo
chondrocyte
comparative transcriptomics
title On the evolutionary relationship between chondrocytes and osteoblasts
title_full On the evolutionary relationship between chondrocytes and osteoblasts
title_fullStr On the evolutionary relationship between chondrocytes and osteoblasts
title_full_unstemmed On the evolutionary relationship between chondrocytes and osteoblasts
title_short On the evolutionary relationship between chondrocytes and osteoblasts
title_sort on the evolutionary relationship between chondrocytes and osteoblasts
topic Bone and Bones
Cartilage
SOX9 Transcription Factor
Evo-Devo
chondrocyte
comparative transcriptomics
url http://journal.frontiersin.org/Journal/10.3389/fgene.2015.00297/full
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