Gene Dosage Compensation in Drosophila Melanogaster

Abstract The period (per) gene is located on the X chromosome of Drosophila melanogaster. Its expression influences biological clocks in this fruit fly, including the one that subserves circadian rhythms of locomotor activity. Like most X-linked genes in Drosophila, per is under the regulatory control of gene dosage compensation. In this study, we assessed the activity of altered or augmented per+ DNA fragments in transformants. Relative expression levels in male and female adults were inferred from periodicities associated with locomotor behavioral rhythms, and by histochemically assessing beta-galactosidase levels in transgenics carrying different kinds of per-lacZ fusion genes. The results suggest that per contains multipartite regulatory information for dosage compensation within the large first intron and also within the 3' half of this genetic locus.

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Gene dosage compensation in metafemales (3X; 2A) of Drosophila

Nature ◽

10.1038/248564a0 ◽

1974 ◽

Vol 248 (5449) ◽

pp. 564-567 ◽

Cited By ~ 29

Author(s):

John C. Lucchesi ◽

John M. Rawls ◽

Gustavo Maroni

Keyword(s):

Dosage Compensation ◽

Gene Dosage

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X chromosome gene dosage compensation in female mammals

Seminars in Developmental Biology ◽

10.1006/sedb.1993.1015 ◽

1993 ◽

Vol 4 (2) ◽

pp. 129-139 ◽

Cited By ~ 9

Author(s):

Giuseppe Borsani ◽

Andrea Ballabio

Keyword(s):

X Chromosome ◽

Dosage Compensation ◽

Gene Dosage ◽

Chromosome Gene

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Dosage compensation of sex-linked genes in Drosophila melanogaster

MGG Molecular & General Genetics ◽

10.1007/bf00267534 ◽

1973 ◽

Vol 126 (3) ◽

pp. 233-245 ◽

Cited By ~ 18

Author(s):

L. Z. Faizullin ◽

V. A. Gvozdev

Keyword(s):

Drosophila Melanogaster ◽

Dosage Compensation

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On the Mode of Gene-Dosage Compensation in Drosophila

Genetics ◽

10.1093/genetics/145.3.729 ◽

1997 ◽

Vol 145 (3) ◽

pp. 729-736

Author(s):

Irina Arkhipova ◽

Jingjing Li ◽

Matthew Meselson

Keyword(s):

X Chromosome ◽

Dosage Compensation ◽

Gene Dosage ◽

Gene Activity ◽

Gene Copy ◽

Drosophila Pseudoobscura ◽

A Site ◽

Reduced Activity ◽

Per Gene

A procedure is described for determining the mode and magnitude of gene-dosage compensation of transformed genes. It involves measurement of the ratio of the activity of a gene inserted at X-linked sites to the activity of the same gene inserted at autosomal sites. Applying the procedure to the Drosophila pseudoobscura Hsp82 gene inserted at ectopic sites in D. melanogaster and taking gene activity as proportional to the amount of transcript per gene copy, we conclude that (1) in both adults and larvae the gene is not compensated at autosomal sites or at a site in β-heterochromatin at the base of the X chromosome and is fully compensated at euchromatic X-chromosomal sites; (2) inappropriate normalization is responsible for a claim that the gene is compensated at autosomal sites; and (3) the observed compensation operates mainly or entirely by heightened activity of X-linked genes in males, rather than by reduced activity in females.

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THE GENETIC BASIS OF DOSAGE COMPENSATION OF ALCOHOL DEHYDROGENASE-1 IN MAIZE

Genetics ◽

10.1093/genetics/97.3-4.625 ◽

1981 ◽

Vol 97 (3-4) ◽

pp. 625-637 ◽

Cited By ~ 2

Author(s):

James A Birchler

Keyword(s):

Alcohol Dehydrogenase ◽

Structural Gene ◽

Dosage Compensation ◽

Genetic Basis ◽

Gene Dosage ◽

Dosage Effect ◽

Gene Dosage Effect ◽

Negative Effect ◽

Higher Eukaryotes ◽

Alcohol Dehydrogenase 1

ABSTRACT The levels of alcohol dehydrogenase (ADH) do not exhibit a structural gene-dosage effect in a one to four dosage series of the long arm of chromosome one (1L) (BIRCHLER19 79). This phenomenon, termed dosage compensation, has been studied in more detail. Experiments are described in which individuals aneuploid for shorter segments were examined for the level of ADH in order to characterize the genetic nature of the compensation. The relative ADH expression in segmental trisomics and tetrasomics of region IL 0.72–0.90, which includes the Adh locus, approaches the level expected from a strict gene dosage effect. Region IL 0.20–0.72 produces a negative effect upon ADH in a similar manner to that observed with other enzyme levels when IL as a whole is varied (BIRCHLEF1I9 79). These and other comparisons have led to the concept that the compensation of ADH results from the cancellation of the structural gene effect by the negative aneuploid effect. The example of ADH is discussed as a model for certain other cases of dosage compensation in higher eukaryotes.

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Aneuploidy and gene expression: is there dosage compensation?

Epigenomics ◽

10.2217/epi-2019-0135 ◽

2019 ◽

Vol 11 (16) ◽

pp. 1827-1837 ◽

Cited By ~ 2

Author(s):

Shihoko Kojima ◽

Daniela Cimini

Keyword(s):

Gene Expression ◽

Dosage Compensation ◽

Current Knowledge ◽

Gene Dosage ◽

Congenital Defects ◽

Gene Products ◽

Epigenetic Changes ◽

Transcript Levels ◽

Compensation Mechanisms ◽

Additional Chromosome

Aneuploidy (i.e., abnormal chromosome number) is the leading cause of miscarriage and congenital defects in humans. Moreover, aneuploidy is ubiquitous in cancer. The deleterious phenotypes associated with aneuploidy are likely a result of the imbalance in the levels of gene products derived from the additional chromosome(s). Here, we summarize the current knowledge on how the presence of extra chromosomes impacts gene expression. We describe studies that have found a strict correlation between gene dosage and transcript levels as wells as studies that have found a less stringent correlation, hinting at the possible existence of dosage compensation mechanisms. We conclude by peering into the epigenetic changes found in aneuploid cells and outlining current knowledge gaps and potential areas of future investigation.

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