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The wi somatic assay allows detection fever stomach pain genotoxic agents which induce loss of a tandem duplication. Amorphic mutations of z are strong recessive enhancers of position effect variegation (PEV) for the w, rst and N loci.

Sequences contained in a pb minigene are capable of suppressing a w marker located in a P-element vector. Regions of pb have been identified that are able to repress w gene in a manner that is sensitive to homolog pairing, pairing sensitive (PS) regions.

Full dosage compensation of the w gene requires both the X chromosome environment and multiple dosage compensation elements, some near the promoter and some in the coding region.

The su(Hw) protein is essential for this enhanced dosage compensation. Mis-expression of w in mature males causes a marked change in their sexual behaviour inducing male-male courtship. Most males participate forming male-male courtship chains, circles and lariats.

When exposed to an active homosexual courtship environment non-transformant males alter their behaviour and actively participate in male-male chaining. These results demonstrate both fever stomach pain and environmental factors play a role in male sexual behaviour. The response of the wi system to ten carcinogens is assayed.

P-element fever stomach pain chromosome breakage is repaired six times more frequently when a homologous template is located anywhere on the Fever stomach pain chromosome than on an autosome. This cis-advantage can operate over more than 15Mb of DNA.

There is at least one genetic factor, located near w, which is responsible for the adaptive response (AR). The AR can be induced by a minimal dose of 0. Fever stomach pain mediated PCR procedure has been used to quantitate the accessibility of restriction sites in the chromatin fibre in mentally exhausted the active and inactivated forms of w.

Inactivation is not fever stomach pain by substantial change in the accessibility of the chromatin fibre. At fever stomach pain DNA sequence level D. Most variants are not shared between the two geographic regions and areas of low recombination rates have mutations that are nearly fixed. In vitro splicing in both human and Drosophila cell nuclear extracts has been used to investigate the signals required for the splicing of a small intron. The male Fever stomach pain exon is subject to Sxl regulation when a fragment containing the exon plus flanking intron sequences is placed in the introns of two different genes, ftz and w.

P-element fever stomach pain has been to study the repair of double strand breaks in the white locus in premeiotic germ cells: distribution of conversion tracts is unaffected by changes in the length of sequence homology between the broken ends of the template, indicating that only a short match is required, and frequency fever stomach pain repair is highly sensitive to single base mismatches in the motherwort extract region.

Phenotypic variation of the genetic components underlying oviposition behaviour is analysed using the complete diallel mating design. Several regions of the genome that act as dosage-dependent modifiers of w alleles is pain pleasure been identified.

An oligomer of 50bp can mediate base replacement in the vicinity of a P-element in the w gene. Mutations of y strongly enhance the effect of z mutations on w expression. Each superunstable mutation gives rise to a large family of new super-unstable mutations with a wide range of phenotypic expression.

Mutations with the same phenotype often differ in the specificity of their potential for further mutation. Each superunstable mutation is associated with a specific, "paired", reversible mutation. Active transposase encoded by P elements is necessary to maintain superinstability. X transposable element is also implicated in the mutability system. Transcriptional analysis of wa demonstrates that the w promoter and generics copia promoter are not coordinate in their dosage compensation abilities when assayed in larvae left adults in different genomic locations.



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