Conservation and Function of Human Oncogene FYN in Drosophila melanogaster
Disciplines
Cancer Biology | Genetics | Molecular Biology
Abstract (300 words maximum)
Many cancers are initiated by the activation of oncogenes, which promote cancer development through a variety of disruptive mechanisms, including excessive proliferation, loss of cell differentiation, and inappropriate cell migration. The mechanisms can be summarized in an organizational system known as the hallmarks of cancer. FYN is a human oncogene implicated in many cancers, especially those of the central nervous system and ovary. FYN encodes a non-receptor tyrosine kinase from the Src tyrosine kinase family, and has been shown in literature to promote proliferation and metastasis. Data from Jia Lab previously demonstrated that human FYN expression in the Drosophila eye resulted in a deleterious effect on eye structure, suggesting potentially conserved functions across species. This project utilized the Gal4-UAS system to express FYN and its closest Drosophila homolog, Src64B, in the eye and ovary of Drosophila melanogaster, to further explore and characterize the mechanisms of FYN. Eye tissue was imaged via light microscopy and scanning electron microscopy. Classic immunostaining was performed on ovarian tissue to determine protein expression, and slides were imaged via confocal microscopy. Our findings suggest that FYN and Src64B exhibit conserved phenotypes when expressed in the eye and ovary. FYN and Src64B expression in the eye demonstrated a conserved rough eye phenotype, including disruption of ommatidia organization and lost or shortened bristles, indicating developmental defects. FYN expression in the Drosophila ovary demonstrated inappropriate accumulation of anterior egg chamber squamous cells without evidence of excessive proliferation. These accumulated squamous cells also exhibited altered expressions of apical, basolateral, and Par-complex polarity factors. Overexpression of Src64B showed similar phenotypes, suggesting that FYN and Src64B function through similar cellular pathways. These results indicate that the conserved oncogenic potential of FYN may be linked to changes in cell polarity signaling, which are considered a hallmark of cancer.
Academic department under which the project should be listed
CSM - Molecular and Cellular Biology
Primary Investigator (PI) Name
Dongyu Jia, Ph.D.
Conservation and Function of Human Oncogene FYN in Drosophila melanogaster
Many cancers are initiated by the activation of oncogenes, which promote cancer development through a variety of disruptive mechanisms, including excessive proliferation, loss of cell differentiation, and inappropriate cell migration. The mechanisms can be summarized in an organizational system known as the hallmarks of cancer. FYN is a human oncogene implicated in many cancers, especially those of the central nervous system and ovary. FYN encodes a non-receptor tyrosine kinase from the Src tyrosine kinase family, and has been shown in literature to promote proliferation and metastasis. Data from Jia Lab previously demonstrated that human FYN expression in the Drosophila eye resulted in a deleterious effect on eye structure, suggesting potentially conserved functions across species. This project utilized the Gal4-UAS system to express FYN and its closest Drosophila homolog, Src64B, in the eye and ovary of Drosophila melanogaster, to further explore and characterize the mechanisms of FYN. Eye tissue was imaged via light microscopy and scanning electron microscopy. Classic immunostaining was performed on ovarian tissue to determine protein expression, and slides were imaged via confocal microscopy. Our findings suggest that FYN and Src64B exhibit conserved phenotypes when expressed in the eye and ovary. FYN and Src64B expression in the eye demonstrated a conserved rough eye phenotype, including disruption of ommatidia organization and lost or shortened bristles, indicating developmental defects. FYN expression in the Drosophila ovary demonstrated inappropriate accumulation of anterior egg chamber squamous cells without evidence of excessive proliferation. These accumulated squamous cells also exhibited altered expressions of apical, basolateral, and Par-complex polarity factors. Overexpression of Src64B showed similar phenotypes, suggesting that FYN and Src64B function through similar cellular pathways. These results indicate that the conserved oncogenic potential of FYN may be linked to changes in cell polarity signaling, which are considered a hallmark of cancer.