Short direct repeats mediate spontaneous high-frequency deletions in DNA of minute virus of mice

1984 ◽  
Vol 4 (10) ◽  
pp. 2239-2242
Author(s):  
A Hogan ◽  
E A Faust

Previous work (E. A. Faust and D. C. Ward, J. Virol. 32:276-292, 1979) revealed a remarkably high rate of spontaneous deletion in viral DNA during lytic infection of cultured murine cells with minute virus of mice (MVM), an autonomous parvovirus. In the present study, we have isolated plasmid and phage recombinants containing MVM DNA inserts bearing deletions and we have determined the DNA sequence spanning three deletion junctions. The deletions, which average 3 kilobases in length, occur between pairs of perfectly homologous 4- to 10-base-pair direct repeats, such that one copy of the repeated sequence is lost, whereas the other remains behind at the deletion junction. When compared, the three sets of direct repeats exhibit no apparent sequence homology and have an A + T content of between 50 and 80%. These results indicate that 4- to 10-base-pair homologies mediate spontaneous deletion formation in the MVM genome and highlight parvoviruses as novel model systems for studies of this ubiquitous pathway of genetic variation.

1984 ◽  
Vol 4 (10) ◽  
pp. 2239-2242 ◽  
Author(s):  
A Hogan ◽  
E A Faust

Previous work (E. A. Faust and D. C. Ward, J. Virol. 32:276-292, 1979) revealed a remarkably high rate of spontaneous deletion in viral DNA during lytic infection of cultured murine cells with minute virus of mice (MVM), an autonomous parvovirus. In the present study, we have isolated plasmid and phage recombinants containing MVM DNA inserts bearing deletions and we have determined the DNA sequence spanning three deletion junctions. The deletions, which average 3 kilobases in length, occur between pairs of perfectly homologous 4- to 10-base-pair direct repeats, such that one copy of the repeated sequence is lost, whereas the other remains behind at the deletion junction. When compared, the three sets of direct repeats exhibit no apparent sequence homology and have an A + T content of between 50 and 80%. These results indicate that 4- to 10-base-pair homologies mediate spontaneous deletion formation in the MVM genome and highlight parvoviruses as novel model systems for studies of this ubiquitous pathway of genetic variation.


1986 ◽  
Vol 59 (3) ◽  
pp. 564-573 ◽  
Author(s):  
C V Jongeneel ◽  
R Sahli ◽  
G K McMaster ◽  
B Hirt

Genetics ◽  
1998 ◽  
Vol 149 (1) ◽  
pp. 143-155 ◽  
Author(s):  
Bruce D McKee ◽  
Kathy Wilhelm ◽  
Cynthia Merrill ◽  
Xiao-jia Ren

Abstract In Drosophila melanogaster, deletions of the pericentromeric X heterochromatin cause X-Y nondisjunction, reduced male fertility and distorted sperm recovery ratios (meiotic drive) in combination with a normal Y chromosome and interact with Y-autosome translocations (T(Y;A)) to cause complete male sterility. The pericentromeric heterochromatin has been shown to contain the male-specific X-Y meiotic pairing sites, which consist mostly of a 240-bp repeated sequence in the intergenic spacers (IGS) of the rDNA repeats. The experiments in this paper address the relationship between X-Y pairing failure and the meiotic drive and sterility effects of Xh deletions. X-linked insertions either of complete rDNA repeats or of rDNA fragments that contain the IGS were found to suppress X-Y nondisjunction and meiotic drive in Xh−/Y males, and to restore fertility to Xh−/T(Y;A) males for eight of nine tested Y-autosome translocations. rDNA fragments devoid of IGS repeats proved incapable of suppressing either meiotic drive or chromosomal sterility. These results indicate that the various spermatogenic disruptions associated with X heterochromatic deletions are all consequences of X-Y pairing failure. We interpret these findings in terms of a novel model in which misalignment of chromosomes triggers a checkpoint that acts by disabling the spermatids that derive from affected spermatocytes.


2021 ◽  
Vol 19 (2) ◽  
pp. 119-125
Author(s):  
E.V. Mikhailova ◽  
◽  
T.K. Chudakova ◽  
D.Yu. Levin ◽  
A.V. Romanovskaya ◽  
...  

Parvovirus (PV) is a widespread infection, despite the fact that this pathogen was discovered only recently. The therapeutic effect of PV, in particular its oncolytic activity, is being actively studied now. Notably, PVs causing infections in animals, such as rat PV H-1, caninae PV, and rodent protoparvovirus (minute virus of mice) suppress oncogenesis in these animals. There is an ex vivo evidence of rat glioblastoma and gliosarcoma sensitivity to PV. The affinity of PV B19 to P-antigen located primarily on the membranes of erythroid cells is crucial for the disease pathogenesis. The teratogenic effect of PV B19 is associated with its ability to infect placental cells (P-antigen is present on the cells of chorionic villi and surface of the trophoblast). PV infection can be acquired or congenital, typical or atypical. The outcome of intrauterine infection with PV B19 largely depends on the gestation age when the infection occurred. Women infected during the second trimester are at higher risk of vertical transmission and severe intrauterine pathology with a poor outcome than those infected during the third trimester. Constant contact with young children significantly increases the risk of PV B19 infection among pregnant women with no immunity to this virus. Serum is the most convenient biomaterial for detecting both PV DNA and virus-specific antibodies. One test for anti-PV IgG using enzyme-linked immunosorbent assay is sufficient to determine the immune status of a patient. Polymerase chain reaction with amniotic fluid is used to diagnose intrauterine infection with PV B19. Blood components and products should be checked for PV B19. High frequency of PV B19 detection in the blood of donors necessitates the development of special measures aimed at prevention of virus transmission. Key words: pregnant women, children, parvovirus B19, parvovirus infection


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