No problem at all! I'm happy to clarify any questions that arise.

We used the term in this thread to distinguish this assembly from contig-only assemblies. If the usage of 'chromosome-scale' was misleading, we apologize, there was no intent to mislead.

We referred to it as chromosome scale as it is assembled into chromosome-level scaffolds spanning entire chromosome arms. We clearly state in the text that it is not telomere-to-telomere (T2T) and does not fully resolve highly repetitive loci like rDNA arrays or centromeres.

Thank you Jakob 😃.

Finally, huge thanks to @juliusbrennecke.bsky.social and the whole Brennecke Group for enduring my long-read obsession! Also worth noting: the Iwasaki and Siomi labs recently published an OSC genome assembly (PMID: 39636727). Exciting to see multiple groups tackling this important resource. (12/12🏁)

Many questions remain about how these patterns emerge and how the right piRNA precursors are selected, but that's a story for another day ;-).
For now, check out the story and explore the genome yourself. We'd love to get your feedback! (11/12)
www.biorxiv.org/content/10.1...

Together, these advances let us explain transposon silencing patterns genome-wide. Cluster content determines piRNA profiles, which in turn dictate which TEs are silenced and which evade the pathway. (10/12)

Earlier work suggested flamenco undergoes splicing. Our data shows that beyond the first intron, the >730 kb transcript appears to be largely unspliced, producing a single continuous precursor feeding the piRNA pathway. (9/12)

Next challenge: determining flamenco's transcriptional extent. We inserted UAS sites upstream and tethered a silencing domain to reduce transcription. The result? piRNA loss extending ≥730 kb downstream, revealing the true scale of this massive locus. (8/12)

So how are these TEs controlled? The flamenco piRNA cluster, OSCs' primary piRNA source, is critical. We resolved the entire locus, bridging an assembly gap in dm6 and it differs not just by a few SNPs: we see major rearrangements and dramatic content changes throughout the locus. (7/12)

How dramatically? OSCs harbor >150 gypsy retrovirus insertions (dm6 has one), while tirant (present in dm6) is absent from OSCs. These post-immortalization changes fundamentally reshape transposon-piRNA dynamics. (6/12)

OSCs show extensive loss-of-heterozygosity regions from events during immortalization as shown previously by @caseybergman.bsky.social (PMID: 34849875) The transposon landscape? It evolved after these LOH events—meaning the insertions we see reflect post-immortalization genome dynamics. (5/12)

Ready to explore? The assembly is live on UCSC Genome Browser with our functional datasets integrated: ChIP-seq, RNA-seq, PRO-seq, and small RNA-seq. Fully annotated and ready for you to go bird watching. (4/12)
genome-euro.ucsc.edu/s/Brennecke%...

Using Oxford Nanopore long reads + Hi-C scaffolding, we generated a chromosome-scale assembly with superior contiguity to dm6 and corrected nearly all those fixed variants, capturing the true OSC genomic sequence. (3/12)

OSCs are widely used for transposon silencing and piRNA studies, but everyone's been mapping to dm6. The problem? OSCs differ by >500K homozygous SNPs and >4,000 structural variants. Try designing siRNAs against SoYb when the reference has 85 homozygous differences in its CDS alone. (2/12)

📌