Figure 5. Model of HOAP[yak] separation-of-function and model of intra-genomic conflict between host telomere proteins and selfish telomeric retrotransposons.

(A) In the presence of the D. yakuba version of HOAP (yellow moon), D. melanogaster telomeres maintain telomere end-protection but lose telomeric retrotransposon silencing and length regulation. We hypothesize that the two defined HOAP functions separate across two multi-protein complexes: HOAP[yak] supports Terminin integrity but disrupts the HOAP-HP1A-HipHop subcomplex. (B) Model of intra-genomic conflict shaping HOAP evolution and telomere retrotransposon evolution. At some timepoint in the past (e.g. along the lineage leading to D. melanogaster), ancestral host telomere proteins successfully contain telomeric retrotransposons ('containment'). Over time, the retrotransposon innovates (gray triangle becomes purple), elongating chromosomes and inserting into non-telomeric locations ('escape'). Fitness costs incurred by the host spurs telomere protein evolution (gray moon becomes a purple moon), restoring control over telomeric retrotransposons ('containment').

Figure 5—figure supplement 1. Reduced HP1a signal at the primary HOAP[yak]-marked telomere cluster in ovarian nurse cells.

(A) Representative images of DNA (white) and HP1a (red) across whole nuclei (left) and HOAP (detected by anti-Flag, green) and HP1a (red) at the primary cluster of telomeres within each nurse cell (right). Dotted circles correspond to the region of interest (ROI) for quantification. (B) Quantification of mean HP1 intensity across HOAP[mel] and HOAP[yak] of 75 nurse cells across 15 individuals ('***' = p-value < 0.0001).

Figure 5—figure supplement 2. Protein alignment of HeT-A Gag consensus from D.melanogaster and D.yakuba.

The two Gag domains share 72% amino acid identity.