A trans-activator on the Drosophila Y chromosome regulates gene expression in the male germ line.

The Y chromosome of Drosophila melanogaster accounts for approximately 13% of a normal male genome and is entirely heterochromatic. It carries six genes required exclusively for spermatogenesis. Here we report a novel activity of the Y chromosome that regulates gene expression in primary spermatocytes. By examining the expression of a reporter gene in X/Y and X/O males, we show that a specific region of the Y long arm carries a trans-activator that regulates transcription in spermatogenesis. In the absence of the Y trans-activator, the level of the reporter expression is greatly reduced in primary spermatocytes and the expression pattern is restricted to young primary spermatocytes. Further analysis shows that the Y trans-activator is dispersed in the h1-h10 region on the Y long arm and is functionally redundant, indicating involvement of the repetitive sequences on the Y chromosome. In addition, the Y trans-activator appears to act in a tissue-specific manner, functioning only in the male germ line. We propose that the Y trans-activator plays an important role in regulating gene expression during spermatogenesis.

Y-Linked male sterile mutations induced by P element in Drosophila melanogaster.

The Y chromosome in Drosophila melanogaster is composed of highly repetitive sequences and is essential only in the male germ line. We employed P-element insertional mutagenesis to induce male sterile mutations in the Y chromosome. By using a combination of two modifiers of position effect variegation, adding an extra Y chromosome and increasing temperature, we isolated 61 P(ry+) elements in the Y chromosome. Six of these Y-linked insertions (approximately 10%) induced male sterile mutations that are mapped to two genes on the long and one on the short arms of the Y chromosome. These mutations are revertible to the wild type in a cell-autonomous and germ-line-dependent manner, consistent with previously defined Y-linked gene functions. Phenotypes associated with these P-induced mutations are similar to those resulting from deletions of the Y chromosome regions corresponding to the male fertility genes. Three alleles of the kl-3 gene on the Y long arm result in loss of the axonemal outer dynein arms in the spermatid tail, while three ks-2 alleles on the Y short arm induce defects at early postmeiotic stages. The recovery of the ms(Y) mutations induced by single P-element insertions will facilitate our effort to understand the structural and functional properties of the Y chromosome.