We examined the heterochromatic binding of GAGA factor and proliferation disrupter (Prod) proteins during the cell cycle in Drosophila melanogaster and sibling species. GAGA factor binding to the brownD ominant AG-rich satellite sequence insertion was seen at metaphase, however, no binding of GAGA factor to AG-rich sequences was observed at interphase in polytene or diploid nuclei. Comparable mitosis-specific binding was found for Prod protein to its target satellite in pericentric heterochromatin. At interphase, these proteins bind numerous dispersed sites in euchromatin, indicating that they move from euchromatin to heterochromatin and back every cell cycle. The presence of Prod in heterochromatin for a longer portion of the cell cycle than GAGA factor suggests that they cycle between euchromatin and heterochromatin independently. We propose that movement of GAGA factor and Prod from high affinity sites in euchromatin occurs upon condensation of metaphase chromosomes. Upon decondensation, GAGA factor and Prod shift from low affinity sites within satellite DNA back to euchromatic sites as a self-assembly process.
The rho family of GTPases has been implicated in regulating changes in cell morphology in response to extracellular signals. We have cloned three widely expressed members of this family from Drosophila melanogaster; a rho homologue (Rho1) and two rac homologues (Rac1 and Rac2). Flies harbouring a Rho1 transgene that is specifically expressed in the eye exhibit a dramatic dose dependent disruption of normal eye development. Flies bearing at least two copies of the transgene display a severe rough eye phenotype characterized by missing secondary and tertiary pigment cells, a substantial reduction in the number of photoreceptor cells and a grossly abnormal morphology of the rhabdomeres. Cell fate determination in the imaginal disc occurs normally and abnormalities become manifest late in pupariation, coincident with the phase when the cells undergo major morphological changes. This phenotype is modified by mutations at several other loci that have been implicated in signal transduction, but not by mutations in ras pathway components.
Hepatitis C virus (HCV) replication at the cellular level is not fully understood. This study describes an optimized system for quantifying replication of HCV in hepatocytes and in liver tissues. A digital image analysis method was developed to quantify signal intensities of HCV genomic and replicative-intermediate1 Symptomatic differences among infected individuals have generated considerable interest in elucidating the pathogenic mechanisms of HCV disease.Previous studies have described the levels of HCV genomes in patient sera in cohorts either on therapeutic drug regimens, untreated, or undergoing liver transplantation. As a whole, these studies have failed to find a consistent relationship between serum titers and the degree of hepatic injury.2-4 The ratios of HCV genome RNA in liver and serum compartments are significantly different among chronically infected patients.2,5-8 These reports suggest that hepatic injury, serum titers, and intrahepatic viral replication do not display a linear relationship during chronic hepatitis C infection.HCV is a positive strand RNA virus that is classified as a Hepacivirus within the Flaviviridae family.9 By analogy with other members of the Flaviviridae, it is assumed that HCV replication requires production of negative strand replicative-intermediate RNA, from which progeny genomic strand RNA is transcribed. The presence of negative strand RNA in cells indicates ongoing HCV replication and synthesis of progeny genomic RNA in these cells. Previously, we and others have used strand-specific in situ hybridization to localize positive strand and negative strand HCV RNAs in infected human liver tissue. 10 The percentage of hepatocytes positive for genomic RNA ranged from 4.8 to 87.6%, 10 -12 whereas those positive for replicative-intermediate RNA ranged from 4 to 25%. 10,13 On visualization, the distribution and abundance of genomic RNA appeared to be different from that of replicative-intermediate RNA, suggesting compartmentalization or regulation of replication may occur.To further characterize HCV replication in liver tissue, we developed an image analysis method to measure quantitative amounts of genomic and replicative-intermediate RNAs in infected liver tissues, and to examine the
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