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Erg is a crucial regulator of endocardial-mesenchymal transformation during cardiac valve morphogenesis.

Vijayaraj P, Le Bras A, Mitchell N, Kondo M, Juliao S, Wasserman M, Beeler D, Spokes K, Aird WC, Baldwin HS, Oettgen P - Development (2012)

Bottom Line: Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes.The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells.We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

ABSTRACT
During murine embryogenesis, the Ets factor Erg is highly expressed in endothelial cells of the developing vasculature and in articular chondrocytes of developing bone. We identified seven isoforms for the mouse Erg gene. Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes. The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells. Homozygous Erg(ΔEx3/ΔEx3) knockout mice are viable, fertile and do not display any overt phenotype. By contrast, homozygous Erg(ΔEx4/ΔEx4) knockout mice are embryonic lethal, which is associated with a marked reduction in endocardial-mesenchymal transformation (EnMT) during cardiac valve morphogenesis. We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.

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ErgEx3 is expressed in the developing joints. (A-H) Whole-mount lacZ staining of Erg+/+ (A,E) and ErgΔEx3/ΔEx3 (B-D,F-H) mouse embryos at E10.5 and E12.5 showing expression in the developing limb (C,G) and skull (D,H). (I-P) lacZ staining of Erg+/+ (I,M) and ErgΔEx3/ΔEx3 (J-L,N-P) mice at E18.5 and P4.
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Figure 4: ErgEx3 is expressed in the developing joints. (A-H) Whole-mount lacZ staining of Erg+/+ (A,E) and ErgΔEx3/ΔEx3 (B-D,F-H) mouse embryos at E10.5 and E12.5 showing expression in the developing limb (C,G) and skull (D,H). (I-P) lacZ staining of Erg+/+ (I,M) and ErgΔEx3/ΔEx3 (J-L,N-P) mice at E18.5 and P4.

Mentions: lacZ staining in ErgΔEx3/+ and ErgΔEx3/ΔEx3 was first observed at E9.5 in the limb bud. At E10.5, expression was seen in the spine and ear regions. By E12.5, lacZ expression was detected in all bony joints, including the skull, spine and limbs (Fig. 3A). To further define the cellular distribution of the lacZ staining in the joints, 10 μm sections of the knee joints from postnatal day (P) 4 pups were counterstained with eosin (Fig. 4). We observed strong lacZ staining only in the articular cartilage in the ErgΔEx3/+ and ErgΔEx3/ΔEx3 P4 mice. This is consistent with the Erg expression pattern previously observed in the mouse by in situ hybridization (Iwamoto et al., 2007). No appreciable morphological changes were observed in the joints of ErgΔEx3/ΔEx3 versus control P7 mice. Radiographs of Erg+/+ and ErgΔEx3/ΔEx3 mice revealed no differences in joint bone structure at 4 or up to 14 months of age (data not shown). Despite the wide expression pattern of Erg isoforms 1-4 in the developing cartilage and joints, the homozygous animals were viable, fertile and did not display any overt phenotype.


Erg is a crucial regulator of endocardial-mesenchymal transformation during cardiac valve morphogenesis.

Vijayaraj P, Le Bras A, Mitchell N, Kondo M, Juliao S, Wasserman M, Beeler D, Spokes K, Aird WC, Baldwin HS, Oettgen P - Development (2012)

ErgEx3 is expressed in the developing joints. (A-H) Whole-mount lacZ staining of Erg+/+ (A,E) and ErgΔEx3/ΔEx3 (B-D,F-H) mouse embryos at E10.5 and E12.5 showing expression in the developing limb (C,G) and skull (D,H). (I-P) lacZ staining of Erg+/+ (I,M) and ErgΔEx3/ΔEx3 (J-L,N-P) mice at E18.5 and P4.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Figure 4: ErgEx3 is expressed in the developing joints. (A-H) Whole-mount lacZ staining of Erg+/+ (A,E) and ErgΔEx3/ΔEx3 (B-D,F-H) mouse embryos at E10.5 and E12.5 showing expression in the developing limb (C,G) and skull (D,H). (I-P) lacZ staining of Erg+/+ (I,M) and ErgΔEx3/ΔEx3 (J-L,N-P) mice at E18.5 and P4.
Mentions: lacZ staining in ErgΔEx3/+ and ErgΔEx3/ΔEx3 was first observed at E9.5 in the limb bud. At E10.5, expression was seen in the spine and ear regions. By E12.5, lacZ expression was detected in all bony joints, including the skull, spine and limbs (Fig. 3A). To further define the cellular distribution of the lacZ staining in the joints, 10 μm sections of the knee joints from postnatal day (P) 4 pups were counterstained with eosin (Fig. 4). We observed strong lacZ staining only in the articular cartilage in the ErgΔEx3/+ and ErgΔEx3/ΔEx3 P4 mice. This is consistent with the Erg expression pattern previously observed in the mouse by in situ hybridization (Iwamoto et al., 2007). No appreciable morphological changes were observed in the joints of ErgΔEx3/ΔEx3 versus control P7 mice. Radiographs of Erg+/+ and ErgΔEx3/ΔEx3 mice revealed no differences in joint bone structure at 4 or up to 14 months of age (data not shown). Despite the wide expression pattern of Erg isoforms 1-4 in the developing cartilage and joints, the homozygous animals were viable, fertile and did not display any overt phenotype.

Bottom Line: Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes.The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells.We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

ABSTRACT
During murine embryogenesis, the Ets factor Erg is highly expressed in endothelial cells of the developing vasculature and in articular chondrocytes of developing bone. We identified seven isoforms for the mouse Erg gene. Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes. The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells. Homozygous Erg(ΔEx3/ΔEx3) knockout mice are viable, fertile and do not display any overt phenotype. By contrast, homozygous Erg(ΔEx4/ΔEx4) knockout mice are embryonic lethal, which is associated with a marked reduction in endocardial-mesenchymal transformation (EnMT) during cardiac valve morphogenesis. We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.

Show MeSH
Related in: MedlinePlus