scholarly journals Tissue-Specific Differences in the Spatial Interposition of X-Chromosome and 3R Chromosome Regions in the Malaria Mosquito Anopheles messeae Fall.

PLoS ONE ◽  
2015 ◽  
Vol 10 (2) ◽  
pp. e0115281 ◽  
Author(s):  
Gleb Artemov ◽  
Semen Bondarenko ◽  
Gleb Sapunov ◽  
Vladimir Stegniy
PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0171290 ◽  
Author(s):  
Semen M. Bondarenko ◽  
Gleb N. Artemov ◽  
Igor V. Sharakhov ◽  
Vladimir N. Stegniy

1977 ◽  
Vol 30 (2) ◽  
pp. 103 ◽  
Author(s):  
Jennifer A Donald ◽  
DW Cooper

The paternal X inactivation system of kangaroos has been investigated in this study by using tritiated uridine-induced chromosome aberrations to distinguish the active from the inactive X. Previous work in eutherian mammals has demonstrated that constitutive heterochromatic chromosome regions are less susceptible to breakage by tritiated uri dine than euchromatic regions. The results of a comparison between the paternal X chromosome of a wallaroo x red kangaroo hybrid female and the two X chromosomes of a red kangaroo female suggested that the facultative heterochromatin of the X is also less susceptible to breakage by this treatment. However there were significantly more breaks of the paternal X in fibroblasts than in lymphocytes of the hybrid female, which agrees with biochemical findings suggesting activation of the paternal X in fibroblasts. Our results strengthen the suggestion of other workers that the reduced number of aberrations in heterochromatin occurs because such breaks occur principally when the DNA and labelled RNA are in apposition during transcription. Some evidence was found of an apparent toxicity effect of the tritiated uridine solution on the cells.


Genetics ◽  
1994 ◽  
Vol 138 (4) ◽  
pp. 1105-1125
Author(s):  
C C Akerib ◽  
B J Meyer

Abstract The primary sex-determination signal of Caenorhabditis elegans is the ratio of X chromosomes to sets of autosomes (X/A ratio). This signal coordinately controls both sex determination and X chromosome dosage compensation. To delineate regions of X that contain counted signal elements, we examined the effect on the X/A ratio of changing the dose of specific regions of X, using duplications in XO animals and deficiencies in XX animals. Based on the mutant phenotypes of genes that are controlled by the signal, we expected that increases (in males) or decreases (in hermaphrodites) in the dose of X chromosome elements could cause sex-specific lethality. We isolated duplications and deficiencies of specific X chromosome regions, using strategies that would permit their recovery regardless of whether they affect the signal. We identified a dose-sensitive region at the left end of X that contains X chromosome signal elements. XX hermaphrodites with only one dose of this region have sex determination and dosage compensation defects, and XO males with two doses are more severely affected and die. The hermaphrodite defects are suppressed by a downstream mutation that forces all animals into the XX mode of sex determination and dosage compensation. The male lethality is suppressed by mutations that force all animals into the XO mode of both processes. We were able to subdivide this region into three smaller regions, each of which contains at least one signal element. We propose that the X chromosome component of the sex-determination signal is the dose of a relatively small number of genes.


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