DNA-protein interactions: genome-wide binding profile assayed for z protein in stage 11 (7.5-9.5 hr) embryos; see BDTNP1_TFBS_z collection report.

RNAi generated by PCR using primers directed to this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R⁺ cells.

z mutations reduce transvection at wupA.

In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.

A proline-rich region in the z protein is essential for transvection and w repression by the z¹ protein.

When z and su(w^sp) mutations are present the action of Ufo is blocked: no significant differences in eye colour detected.

z protein is required for efficient silencing by the iab-7PRE of the Fab-7 element.

Studies of Ubx-Ecol\lacZ promoter constructs show that binding of z protein to either the proximal enhancer of Ubx or to the BXD enhancer element of Ubx does not require the presence of the other element. However, significant transcription is observed only when both elements are present and bound by z.

Mow changes the expression of w. The action of z on w is not interrupted by Mow, but the action of Mow is blocked by z.

The Ubx gene has redundant cis-regulatory elements, which apparently contain binding sites for factors that share the function of the z gene product. z and Trl have an overlapping function in regulating Ubx. The z product binds at equal levels to Ubx promoter constructs (which it activates) as to the endogenous Ubx gene (which it redundantly regulates). z is significantly active in the wild-type situation.

Three assays (z-w, wⁱ and wing spot) are used to evaluate the genotoxic response of five chemicals classified as genotoxic non-carcinogens, chemicals significantly increase the frequency of mutant clones.

Transvection of iab5,6,7 is z independent.

Amorphic mutations of z are strong recessive enhancers of position effect variegation (PEV) for the w, rst and N loci. Results propose that z is important for the opening and stabilising of chromatin domains, a step in gene determination and the establishment of cell memory. Chromatin domains that have been structurally modified by chromosomal rearrangement or by insertion of a transposable element are particularly sensitive to the absence or modification of the z protein.

z blocks the action of Wow on w, but only in the most extreme cases.

The effect of mutations in the z locus on mutagenesis in the y^2ns sc^me double superunstable system has been analysed.

z gene product functions as part of a complex that stimulates transcription by changing chromatin conformation to establish and maintain transcriptionally active domains.

In vivo crosslinking has been used to directly measure DNA binding of z. z protein binds to short DNA elements within a target promoter, no binding was seen to non-target genes.

The assembly of the z gene product into multimeric forms is an orderly, stepwise process which can be arrested at intermediate stages by mutations affecting the integrity or configuration of heptad repeats. The formation of large aggregates is strictly correlated with the ability to suppress w gene expression in the eye. Direct interactions between z protein molecules in vivo as well as in vitro have been demonstrated.

The z protein binds to DNA in a highly cooperative manner which depends on its ability to form multimers which can interact simultaneously with multiple recognition sequences. The DNA binding domain alone is insufficient for stimulation of w, suggesting that another region of the protein is required for proper function in vivo.

There is considerable overlap of chromosomal binding sites for Psc, Su(z)2, z, Pc and the polyhomeotic proteins.

In vitro studies of mutated and deleted z proteins indicate that a sequence in the z protein that resembles the DNA recognition helix of homeodomain proteins is essential for DNA binding activity. The C-terminal domain of the z protein is responsible for the extensive aggregation properties of the z protein that are required for its role in transvection phenomena.

Mutations of y strongly enhance the effect of z mutations on w expression.

z directly and potently activates Ubx transcription in vivo.

Measurements of the activity of GTP cyclohydrolase demonstrate a much lower level of substrate utilization in z-eyed flies than in wild type flies.

Molecular analysis has identified z binding sites in the eye, but not the testes, enhancer of the w gene. Overlap of these sites is responsible for the z-w interaction.

The unstable z-w assay was used to compare mutation rates in germinal and somatic cells. Formaldehyde and methylmethane sulphonate induce mutations in larval and adult feeding in somatic and germinal cells: methylmethane sulphonate causes an elevated frequency of mutations in somatic and germinal cells and formaldehyde only causes somatic mutations.

The mutagenicity of the antifungal preservative methyl p-hydrobenzoate has been analysed using the z eye spot test.

z-w assay is highly sensitive to carcinogenic compounds.

ZESTE genetic test system is used to investigate whether chrysotile and amosite asbestos induces germ-line aneuploidy - both asbestos have germ-line effects.

Dichloroacetonitrile, not dibromoacetonitrile, is an effective inducer of aneuploidy in oocytes using the ZESTE genetic test system.

FIX and ZESTE systems permit rapid and efficient detection of exceptional offspring derived from aneuploid female germ cells. The system differs in response to different chemicals.

ZESTE system is used to monitor induction of sex chromosome aneuploidy following inhalation exposure to nitriles - nitriles disrupt chromosome segregation in oocytes.

When z is effective against w the Inr-a interaction is blocked.

z interacts with w in an eye specific manner.

zeste deleted females have a dull reddish/brown eye colour. Despite the eye colour morphology is normal, females are fertile with almost normal levels of fecundity to give zeste deficient progeny. P elements carrying a wild type copy of z were able to rescue the mutant eye colour to wild type, but did not correct lowered viability. Results suggest that z may not be essential for the viability or female fertility.

Sequence elements present in the region from 1.1 to 1.9kb upstream from the 5' end of the w transcript are required for the interaction of w with z.

Novel class of z mutations have been selected and analyzed.

Inversions, translocations and transpositions with breaks in 3C3, induced as derivatives of z¹ chromosomes carrying tandem duplications of w⁺, result in a range of zeste phenotypes in males and females, the eye colors being zeste, zeste variegated, zeste halo and wild type (Green, 1967; Green, 1984). E(z) and Su(z) loci have been described (Green, 1967; Kalisch and Rasmuson, 1974; Persson, 1976).

The regulatory gene zeste interacts with the white locus as well as with the bithorax and decapentaplegic complexes, changing the phenotypic expression of these loci. z¹ was the first mutant allele identified (Gans, 1948; Gans, 1953); the homo- or hemizygotes of this neomorphic mutant show a lemon yellow eye color when carrying two paired copies of w⁺ or of the rightmost w⁺ alleles <up>as in z¹ w⁺/z¹ w⁺ females or z¹/Y males with a w⁺ duplication (Jack and Judd, 1979)</up>. z¹ w⁺/Y males without the duplication, z¹/z¹ females heterozygous for a w allele belonging to one of the right-hand (zeste-suppressing) subloci, or z⁺/z¹ females are wild type. An intralocus duplication for a right sublocus of white produces mottling in z¹ males. z¹ eye color develops autonomously in mosaics and in eye-disk transplants. It is not affected by the number of Y chromosomes in the genotype. A third chromosome mutant wo interacts with z¹ or z^58g to lighten eye color, producing z/z;wo/wo white-eyed females and z/Y;wo/wo males with a slight deviation from wild-type eye color (Rayle, 1969; Kaufman et al., 1973). z¹ has no effect on the expression of the white gene in ocelli, testes, or larval Malpighian tubules. The first z^a mutant was also identified by Gans. These mutants are wild type in z^a/Y males and z^a/z^a, z^a/Df(1)z, and z⁺/z^a females. The heteroallelic combination of z¹/z^a, however, results in yellow-eyed flies. Complementation between w^sp1 and other white alleles does not occur in z^a mutants, although it does occur in z⁺ or z¹ flies (Babu and Bhat, 1980). z^a-type alleles, including z^ae(bx), as well as the partial revertant of z¹, z^11G3, enhance the mutant phenotype of certain heteroallelic combinations of BXC alleles that show transvection (partial complementation) when paired; z⁺ and z¹, however, do not affect these BXC alleles (Kaufman et al., 1973; Gelbart and Wu, 1982; Mariani et al., 1985; Pirrotta et al., 1987). All zeste mutant alleles tested enhance certain heteroallelic mutant combinations that show transvection in dpp (Gelbart and Wu, 1982). The z^op mutants (Lifschytz and Green, 1984), unlike z¹, require only one copy of w⁺ for expression of a zeste eye color in homo- and hemizygotes. Heterozygotes over z⁺ are zeste if they have two copies of w⁺, but are wild type if there is only one copy. Another mutant, z^v77h, requires only one copy of w⁺ in males. The eyes are brown variegated in hemi- and homozygous z^v77h females and z^v77h/Y males, but wild type in homozygous z^v77h Dp(1;1)w⁺2 females and z^v77h Dp(1;1)w⁺2/Y males, this allele responding to an increase in w⁺ dosage in a manner contrary to that of z¹ (Green, 1984). Diepoxy-butane-induced mutations (including multilocus deletions) have been generated in an attempt to obtain a null allele of zeste (Goldberg, Colvin and Mellin, 1989). Some of the females that were completely deficient for z <up>Df(1)z-deb3/Df(1)z-deb3, for example</up> survived and were fertile, indicating that the product of the zeste gene is not required for viability or female fertility.