Heterochromatin of the Drosophila melanogaster Y chromosome as modifier of position effect variegation: The time of its action

1977 ◽  
Vol 151 (2) ◽  
pp. 111-114 ◽  
Author(s):  
Hans Joachim Becker ◽  
Wilfried Janning
Genome ◽  
2002 ◽  
Vol 45 (6) ◽  
pp. 1025-1034 ◽  
Author(s):  
M L Balasov

The position effect of the AR 4-24 P[white, rosy] transposon was studied at cytological position 60F. Three copies of the transposon (within ~50-kb region) resulted in a spatially restricted pattern of white variegation. This pattern was modified by temperature and by removal of the Y chromosome, suggesting that it was due to classical heterochromatin-induced position effect variegation (PEV). In contrast with classical PEV, extra dose of the heterochromatin protein 1 (HP1) suppressed white variegation and one dose enhanced it. The effect of Pc-G, trx-G, and other PEV suppressors was also tested. It was found that E(Pc)1, TrlR85, and mutations of Su(z)2C relieve AR 4-24- silencing and z1 enhances it. To explain the results obtained with these modifiers, it is proposed that PEV and telomeric position effect can counteract each other at this particular cytological site.Key words: position effect variegation, heterochromatin protein 1, Drosophila melanogaster.


Genetics ◽  
1989 ◽  
Vol 122 (4) ◽  
pp. 793-800 ◽  
Author(s):  
P Dimitri ◽  
C Pisano

Abstract Position effect variegation results from chromosome rearrangements which translocate euchromatic genes close to the heterochromatin. The euchromatin-heterochromatin association is responsible for the inactivation of these genes in some cell clones. In Drosophila melanogaster the Y chromosome, which is entirely heterochromatic, is known to suppress variegation of euchromatic genes. In the present work we have investigated the genetic nature of the variegation suppressing property of the D. melanogaster Y chromosome. We have determined the extent to which different cytologically characterized Y chromosome deficiencies and Y fragments suppress three V-type position effects: the Y-suppressed lethality, the white mottled and the brown dominant variegated phenotypes. We find that: (1) chromosomes which are cytologically different and yet retain similar amounts of heterochromatin are equally effective suppressors, and (2) suppression effect is positively related to the size of the Y chromosome deficiencies and fragments that we tested. It increases with increasing amounts of Y heterochromatin up to 60-80% of the entire Y, after which the effect reaches a plateau. These findings suggest suppression is a function of the amount of Y heterochromatin present in the genome and is not attributable to any discrete Y region.


Genetics ◽  
1978 ◽  
Vol 88 (3) ◽  
pp. 487-497
Author(s):  
William J Morrison ◽  
Ross J MacIntyre

ABSTRACT A translocation in which a segment of chromosome 3 is inserted into the Y chromosome was found to contain the acid phosphatase-1 gene (Acph-1). In flies hyperploid for that gene, acid phosphatase-1 levels are proportional to the dose of the gene. The locus is placed within the salivary chromosome subdivisions 99D and 99E on the basis of its inclusion in the translocated segment and on the previous placement of the claret locus. Several chromosomal rearrangements involving heterochromatic breakpoints and euchromatic breakpoints adjacent to 99D-99E were tested for possible position-effect variegation of acid phosphatase-1. No decrease in the synthesis of the electrophoretic subunit encoded by the relocated gene was observed within any of the rearrangements.


Genetics ◽  
2000 ◽  
Vol 154 (2) ◽  
pp. 657-668 ◽  
Author(s):  
Randy Mottus ◽  
Richard E Sobel ◽  
Thomas A Grigliatti

Abstract For many years it has been noted that there is a correlation between acetylation of histones and an increase in transcriptional activity. One prediction, based on this correlation, is that hypomorphic or null mutations in histone deacetylase genes should lead to increased levels of histone acetylation and result in increased levels of transcription. It was therefore surprising when it was reported, in both yeast and fruit flies, that mutations that reduced or eliminated a histone deacetylase resulted in transcriptional silencing of genes subject to telomeric and heterochromatic position effect variegation (PEV). Here we report the first mutational analysis of a histone deacetylase in a multicellular eukaryote by examining six new mutations in HDAC1 of Drosophila melanogaster. We observed a suite of phenotypes accompanying the mutations consistent with the notion that HDAC1 acts as a global transcriptional regulator. However, in contrast to recent findings, here we report that specific missense mutations in the structural gene of HDAC1 suppress the silencing of genes subject to PEV. We propose that the missense mutations reported here are acting as antimorphic mutations that “poison” the deacetylase complex and propose a model that accounts for the various phenotypes associated with lesions in the deacetylase locus.


Genetics ◽  
1997 ◽  
Vol 145 (4) ◽  
pp. 945-959
Author(s):  
Vett K Lloyd ◽  
Donald A Sinclair ◽  
Thomas A Grigliatti

Position effect variegation (PEV) results from the juxtaposition of a euchromatic gene to heterochromatin. In its new position the gene is inactivated in some cells and not in others. This mosaic expression is consistent with variability in the spread of heterochromatin from cell to cell. As many components of heterochromatin are likely to be produced in limited amounts, the spread of heterochromatin into a normally euchromatic region should be accompanied by a concomitant loss or redistribution of the protein components from other heterochromatic regions. We have shown that this is the case by simultaneously monitoring variegation of a euchromatic and a heterochromatic gene associated with a single chromosome rearrangement. Secondly, if several heterochromatic regions of the genome share limited components of heterochromatin, then some variegating rearrangements should compete for these components. We have examined this hypothesis by testing flies with combinations of two or more different variegating rearrangements. Of the nine combinations of pairs of variegating rearrangements we studied, seven showed nonreciprocal interactions. These results imply that many components of heterochromatin are both shared and present in limited amounts and that they can transfer between chromosomal sites. Consequently, even nonvariegation portions of the genome will be disrupted by re-allocation of heterochromatic proteins associated with PEV. These results have implications for models of PEV.


1987 ◽  
Vol 210 (3) ◽  
pp. 429-436 ◽  
Author(s):  
G. Reuter ◽  
J. Gausz ◽  
H. Gyurkovics ◽  
B. Friede ◽  
R. Bang ◽  
...  

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