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Microbead Implantation in the Zebrafish Embryo
Published on: July 30, 2015
Insulin-like growth factor signaling regulates zebrafish embryonic growth and development by promoting cell survival
P J Schlueter1, G Peng, M Westerfield
1Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Abstract:
Although much is known about the global effects of insulin-like growth factor 1 receptor (IGF1R)-mediated signaling on fetal growth and the clinical manifestations resulting from IGF/IGF1R deficiencies, we have an incomplete understanding of the cellular actions of this essential pathway during vertebrate embryogenesis. In this study, we inhibited IGF1R signaling during zebrafish embryogenesis using antisense morpholino oligonucleotides or a dominant-negative IGF1R fusion protein. IGF1R inhibition resulted in reduced embryonic growth, arrested development and increased lethality. IGF1R-deficient embryos had significant defects in the retina, inner ear, motoneurons and heart. No patterning abnormalities, however, were found in the brain or other embryonic tissues. At the cellular level, IGF1R inhibition increased caspase 3 activity and induced neuronal apoptosis. Coinjection of antiapoptotic bcl2-like mRNA attenuated the elevated apoptosis and rescued the retinal and motoneuron defects, but not the developmental arrest. Subsequent cell cycle analysis indicated an increased percentage of cells in G1 and a decreased percentage in S phase in IGF1R-deficient embryos independent of apoptosis. These results provide novel insight into the cellular basis of IGF1R function and show that IGF1R signaling does not function as an anteriorizing signal but regulates embryonic growth and development by promoting cell survival and cell cycle progression.
Insights
Insulin-like growth factor 1 receptor (IGF1R) signaling is crucial for zebrafish embryonic development. Inhibiting IGF1R impairs growth and cell survival, highlighting its role in cell cycle progression and organ development.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- Insulin-like growth factor 1 receptor (IGF1R) signaling impacts fetal growth and development.
- Cellular mechanisms of IGF1R in vertebrate embryogenesis are not fully understood.
Purpose of the Study:
- To investigate the cellular functions of IGF1R signaling during zebrafish embryogenesis.
- To elucidate the role of IGF1R in embryonic growth, development, and cell survival.
Main Methods:
- Inhibition of IGF1R signaling using antisense morpholino oligonucleotides and a dominant-negative IGF1R fusion protein in zebrafish embryos.
- Assessment of embryonic growth, survival, and specific organ development (retina, inner ear, motoneurons, heart).
- Analysis of apoptosis using caspase 3 activity and cell cycle progression.
Main Results:
- IGF1R inhibition led to reduced embryonic growth, developmental arrest, increased lethality, and defects in the retina, inner ear, motoneurons, and heart.
- IGF1R deficiency increased caspase 3 activity and neuronal apoptosis, which was partially rescued by bcl2-like mRNA.
- Cell cycle analysis revealed altered G1 and S phase distribution, independent of apoptosis.
Conclusions:
- IGF1R signaling is essential for embryonic growth and development in zebrafish.
- IGF1R promotes cell survival and cell cycle progression, crucial for normal embryogenesis.
- IGF1R does not function as an anteriorizing signal but is vital for developmental processes.
