Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.

E26 transformation specific (ETS) family transcription factors are expressed during embryogenesis and are involved in various cellular processes such as proliferation, migration, differentiation, angiogenesis, apoptosis, and survival of cellular lineages to ensure appropriate development. Dysregulat...

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Main Authors: Swapnalee Sarmah, Matthew R Hawkins, Priyadharshini Manikandan, Mark Farrell, James A Marrs
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2022-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0276255
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author Swapnalee Sarmah
Matthew R Hawkins
Priyadharshini Manikandan
Mark Farrell
James A Marrs
author_facet Swapnalee Sarmah
Matthew R Hawkins
Priyadharshini Manikandan
Mark Farrell
James A Marrs
author_sort Swapnalee Sarmah
collection DOAJ
description E26 transformation specific (ETS) family transcription factors are expressed during embryogenesis and are involved in various cellular processes such as proliferation, migration, differentiation, angiogenesis, apoptosis, and survival of cellular lineages to ensure appropriate development. Dysregulated expression of many of the ETS family members is detected in different cancers. The human ELF3, a member of the ETS family of transcription factors, plays a role in the induction and progression of human cancers is well studied. However, little is known about the role of ELF3 in early development. Here, the zebrafish elf3 was cloned, and its expression was analyzed during zebrafish development. Zebrafish elf3 is maternally deposited. At different developmental stages, elf3 expression was detected in different tissue, mainly neural tissues, endoderm-derived tissues, cartilage, heart, pronephric duct, blood vessels, and notochord. The expression levels were high at the tissue boundaries. Elf3 loss-of-function consequences were examined by using translation blocking antisense morpholino oligonucleotides, and effects were validated using CRISPR/Cas9 knockdown. Elf3-knockdown produced short and bent larvae with notochord, craniofacial cartilage, and fin defects. The extracellular matrix (ECM) in the fin and notochord was disorganized. Neural defects were also observed. Optic nerve fasciculation (bundling) and arborization in the optic tectum were defective in Elf3-morphants, and fragmentation of spinal motor neurons were evident. Dysregulation of genes encoding ECM proteins and matrix metalloprotease (MMP) and disorganization of ECM may play a role in the observed defects in Elf3 morphants. We conclude that zebrafish Elf3 is required for epidermal, mesenchymal, and neural tissue development.
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spelling doaj.art-25267f5ea4884043ae3833520aa8f6b52023-05-25T05:31:37ZengPublic Library of Science (PLoS)PLoS ONE1932-62032022-01-011711e027625510.1371/journal.pone.0276255Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.Swapnalee SarmahMatthew R HawkinsPriyadharshini ManikandanMark FarrellJames A MarrsE26 transformation specific (ETS) family transcription factors are expressed during embryogenesis and are involved in various cellular processes such as proliferation, migration, differentiation, angiogenesis, apoptosis, and survival of cellular lineages to ensure appropriate development. Dysregulated expression of many of the ETS family members is detected in different cancers. The human ELF3, a member of the ETS family of transcription factors, plays a role in the induction and progression of human cancers is well studied. However, little is known about the role of ELF3 in early development. Here, the zebrafish elf3 was cloned, and its expression was analyzed during zebrafish development. Zebrafish elf3 is maternally deposited. At different developmental stages, elf3 expression was detected in different tissue, mainly neural tissues, endoderm-derived tissues, cartilage, heart, pronephric duct, blood vessels, and notochord. The expression levels were high at the tissue boundaries. Elf3 loss-of-function consequences were examined by using translation blocking antisense morpholino oligonucleotides, and effects were validated using CRISPR/Cas9 knockdown. Elf3-knockdown produced short and bent larvae with notochord, craniofacial cartilage, and fin defects. The extracellular matrix (ECM) in the fin and notochord was disorganized. Neural defects were also observed. Optic nerve fasciculation (bundling) and arborization in the optic tectum were defective in Elf3-morphants, and fragmentation of spinal motor neurons were evident. Dysregulation of genes encoding ECM proteins and matrix metalloprotease (MMP) and disorganization of ECM may play a role in the observed defects in Elf3 morphants. We conclude that zebrafish Elf3 is required for epidermal, mesenchymal, and neural tissue development.https://doi.org/10.1371/journal.pone.0276255
spellingShingle Swapnalee Sarmah
Matthew R Hawkins
Priyadharshini Manikandan
Mark Farrell
James A Marrs
Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.
PLoS ONE
title Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.
title_full Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.
title_fullStr Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.
title_full_unstemmed Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.
title_short Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.
title_sort elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis
url https://doi.org/10.1371/journal.pone.0276255
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