Proliferative genes induce somatic pairing defects in Drosophila melanogaster and allow replication.
Drosophila tumor forming lines (malignant brain tumor, lethal giant larvae, discs large, brain tumor, and tumor suppressor gene) exhibit incomplete somatic pairing of specific regions in the salivary gland chromosomes, indicating that excessive cell proliferation correlates with somatic pairing defects in Drosophila. Alleles of malignant brain tumor enhancing the frequency of cell divisions exhibit melanizing tumors in the larvae. The giant chromosomes are defective in somatic pairing, indicating that a functional component of the chromosomes is influenced. Genes at different sites are affected, but the similarity of the phenotypes and complex complementation pattern reveals that their functions are interrelated. In the brain of malignant brain tumor recombinants and mutants in proliferative genes, polytene cells appear; wildtype does not amplify DNA in brain tissue cells. Thus, mutant proliferative genes induce the S-phase and allow replication of DNA.
Riede
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BL-Institut für Neurobiologie, Magdeburg, Germany.
D000818:Animals; D001932:Brain Neoplasms / Q000235:genetics; D002455:Cell Division; D002874:Chromosome Mapping; D002875:Chromosomes / Q000502:physiology / Q000648:ultrastructure*; D004261:DNA Replication; D004331:Drosophila melanogaster / Q000235:genetics*; D005816:Genetic Complementation Test; D017404:In Situ Hybridization, Fluorescence; D008545:Melanoma / Q000235:genetics; D009374:Neoplasms, Experimental / Q000235:genetics*; D011995:Recombination, Genetic