Figure 1.
TSE is restricted to the female germline.
Males from lines carrying various tested euchromatic P-lacZ enhancer-trap transgenes expressed in different tissues were crossed with females devoid of P-transgenes (M females) or with females carrying the telomeric silencer P-1152. G1 individuals were stained overnight for lacZ activity. A–F, adult ovaries; G–H, adult testis; I–J, third instar larvae salivary glands (full arrow) and fat body (dashed arrow). The staining observed in the larval brain is not discussed in the present analysis since the P-1152 transgene alone produces staining in this tissue. The enhancer-traps tested as targets and introduced by the fathers are indicated on the figure (on the left) and their structures and locations are described in the “Material and Methods”.
Figure 2.
TSE occurs in third instar larvae and presents the same properties as in adults.
Different crosses were performed between individuals from M or P-1152 lines and individuals from lines carrying various euchromatic P-lacZ enhancer-trap transgenes expressed in different tissues. Imaginal discs or gonads from G1 third instar larvae were stained overnight for lacZ activity. The tissue is indicated on the figure together with the cross (above) and the enhancer-trap used (on the left). ptc-lacZ and sd-lacZ are enhancer trap in the patched and scalloped genes, respectively. BC69 and BQ16 are expressed in the germline of the two sexes and are described in the “Material and Methods”. Pictures are not to scale.
Table 1.
Capacity of P transgenes to induce Trans-Silencing Effect.
Figure 3.
Silencers inserted at different telomeres exhibit a maternal effect.
The two reciprocal crosses were performed between individuals carrying the euchromatic P-otu-lacZ transgene (P-Co1), used as the TSE target, and lines carrying a telomeric silencer transgene inserted in TAS. As an expression control, P-Co1 individuals were crossed with Canton M individuals (devoid of P sequences). In each case, ovaries from G1 females were stained overnight for lacZ activity. The percentage of repressed egg chambers (% of TSE) is given with the total number of egg chambers counted in parenthesis. The transgenes tested as silencers are indicated on the figure (on the left) and their structures and locations are described in the text and in Figure S1.
Figure 4.
Functional interaction between silencers located in TAS at non-homologous telomeres: a silencer inserted at the 3R chromosome arm telomere transmits a maternal component which stimulates the repressive properties of a silencer located on the X-chromosome telomere.
Genotypes are given for chromosomes 1 and 3. “A” females, hemizygous for the P-1155 telomeric silencer locus on the third chromosome, were established by crossing homozygous P-1155 females and males carrying the balancer chromosome TM3-Sb (marked by the dominant Stubble mutation). These “A” females were crossed with males carrying the P-Co1 euchromatic P-lacZ as target in order to recover the “B” and “C” females having inherited, or not, P-1155. “A” females were also crossed with P-1152; P-lacZ-target males in order to recover the “D” females having inherited P-1152 from the father and the “F” females having inherited the two telomeric silencers. P-1152; P-lacZ-target males were also crossed with females devoid of P-transgenes producing “E” females genotypically similar to “D” females, except that they have inherited a naive cytoplasm, whereas, “D” females have inherited a “P-1155” cytoplasm. “B–F” females were scored for TSE. “G” females show the expression control for the target. The percentage of repressed egg chambers (% of TSE) is given with the total number of egg chambers counted in parenthesis.
Figure 5.
Functional interaction between silencers located in TAS at non-homologous telomeres: reciprocal interaction between the silencers located at the X and 3R arm telomeres.
Presentation is similar to that in Figure 4. “A” females, hemizygous for the P-1152 telomeric silencer locus on the X chromosome and carrying the P-Co1 euchromatic target, were established by crossing homozygous P-1152; P-Co1 females and males carrying the balancer chromosomes Muller-5 (M5) and TM3. These “A” females were crossed with males devoid of P-transgenes in order to recover the “B” and “C” females having inherited, or not, P-1152. “A” females were also crossed with P-1155 males in order to recover the “D” females having inherited P-1155 from the father and “F” females having inherited the two telomeric silencers. P-1155 males were also crossed with P-Co1 females producing “E” females genotypically similar to “D” females, except that they have inherited a naive cytoplasm, whereas, “D” females have inherited a “P-1152” cytoplasm. “B–F” females were scored for TSE. “G” females show the expression control for the target.
Figure 6.
Maternal inheritance of TSE does not require the presence of the target.
The two reciprocal crosses were performed between P-1152 and individuals devoid of P-transgenes and carrying the Muller-5 chromosome marked with Bar. G1 females have the same genotype, but have inherited different cytoplasms. These G1 females were crossed with males carrying an euchromatic P-lacZ as target and the capacity of G2 females to repress this target was measured after overnight lacZ staining. The experiment was performed with two different P-lacZ enhancer traps as targets (BQ16 and BC69). The percentage of TSE is given with the total number of egg chambers scored in parenthesis.
Table 2.
Capacity of a telomeric locus to repress two target transgenes inserted at allelic or non-allelic positions.