Dataset Information

Sema3D and Sema7A have distinct expression patterns in chick embryonic development.

ABSTRACT: By RT-PCR, we isolated a partial cDNA clone for the chick Semaphorin7A (Sema7A) gene. We further analyzed its expression patterns and compared them with those of the Sema3D gene, in chick embryonic development. Sema3D and Sema7A appeared to be expressed in distinct cell populations. In mesoderm-derived structures, Sema7A expression was detected in the newly formed somites, whereas Sema3D expression was found in the notochord. In ectoderm-derived tissues, Sema3D is expressed broadly in the surface ectoderm, lens and nasal placodes. Sema3D is also expressed in the developing nervous system including diencephalon, dorsal neural tube, optical and otic vesicles. In the limb bud, Sema3D expression was found throughout the ectoderm excluding the apical ectoderm ridge (AER), where Sema7A is concentrated. Although both genes appeared to be expressed in the migrating neural crest cells, Sema3D expression is limited to neural crest cells migrating out of the midbrain/hindbrain regions, while Sema7A expression is widespread in both cranial and trunk neural crest cells.

SUBMITTER: Bao ZZ

PROVIDER: S-EPMC1564195 | biostudies-literature | 2006 Aug

REPOSITORIES: biostudies-literature

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Sema3D and Sema7A have distinct expression patterns in chick embryonic development.

Bao Zheng-Zheng ZZ Jin Zhe Z

Developmental dynamics : an official publication of the American Association of Anatomists 20060801 8

By RT-PCR, we isolated a partial cDNA clone for the chick Semaphorin7A (Sema7A) gene. We further analyzed its expression patterns and compared them with those of the Sema3D gene, in chick embryonic development. Sema3D and Sema7A appeared to be expressed in distinct cell populations. In mesoderm-derived structures, Sema7A expression was detected in the newly formed somites, whereas Sema3D expression was found in the notochord. In ectoderm-derived tissues, Sema3D is expressed broadly in the surfac ...[more]

PMID: 16804892

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Project description:The heart is the first functioning organ to develop during embryogenesis. The formation of the heart is a tightly regulated and complex process, and alterations to its development can result in congenital heart defects. Mutations in sarcomeric proteins, such as alpha myosin heavy chain and cardiac alpha actin, have now been associated with congenital heart defects in humans, often with atrial septal defects. However, cardiac troponin T (cTNT encoded by gene TNNT2) has not. Using gene-specific antisense oligonucleotides, we have investigated the role of cTNT in chick cardiogenesis. TNNT2 is expressed throughout heart development and in the postnatal heart. TNNT2-morpholino treatment resulted in abnormal atrial septal growth and a reduction in the number of trabeculae in the developing primitive ventricular chamber. External analysis revealed the development of diverticula from the ventricular myocardial wall which showed no evidence of fibrosis and still retained a myocardial phenotype. Sarcomeric assembly appeared normal in these treated hearts. In humans, congenital ventricular diverticulum is a rare condition, which has not yet been genetically associated. However, abnormal haemodynamics is known to cause structural defects in the heart. Further, structural defects, including atrial septal defects and congenital diverticula, have previously been associated with conduction anomalies. Therefore, to provide mechanistic insights into the effect that cTNT knockdown has on the developing heart, quantitative PCR was performed to determine the expression of the shear stress responsive gene NOS3 and the conduction gene TBX3. Both genes were differentially expressed compared to controls. Therefore, a reduction in cTNT in the developing heart results in abnormal atrial septal formation and aberrant ventricular morphogenesis. We hypothesize that alterations to the haemodynamics, indicated by differential NOS3 expression, causes these abnormalities in growth in cTNT knockdown hearts. In addition, the muscular diverticula reported here suggest a novel role for mutations of structural sarcomeric proteins in the pathogenesis of congenital cardiac diverticula. From these studies, we suggest TNNT2 is a gene worthy of screening for those with a congenital heart defect, particularly atrial septal defects and ventricular diverticula.

Dataset Information

Sema3D and Sema7A have distinct expression patterns in chick embryonic development.

Publications

Sema3D and Sema7A have distinct expression patterns in chick embryonic development.

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