Figure 4. FPA-dependent alternative polyadenylation of NLR transcripts.

FPA controls (A) readthrough and chimeric RNA formation at AT1G58848 (unique mapping of short Helicos DRS reads was not possible due to the high homology of AT1G58848 to tandemly duplicated NLR loci in the same cluster); (B) intronic polyadenylation at AT1G69550, resulting in transcripts encoding a protein with a truncated LRR domain; (C) exonic polyadenylation at AT2G14080, resulting in stop-codonless transcripts; and (D) exonic polyadenylation at AT5G40060, resulting in transcripts encoding a TIR-domain-only protein due to an upstream ORF.

Figure 4—figure supplement 1. NLR genes with FPA-dependent alternative polyadenylation are found in hotspots of rearrangements.

Boxplot showing the synteny diversity, calculated from seven diverse A. thaliana accessions (Jiao and Schneeberger, 2020), of expressed NLR genes with and without FPA-sensitive alternative polyadenylation.

Figure 4—figure supplement 2. Loss of FPA function causes chimeric RNA formation at AT1G63730 and AT1G63740 NLR loci.

Gene track showing chimeric RNA formation at the AT1G63730 gene locus, as detected with Illumina RNA-Seq, Helicos DRS, and Nanopore DRS.

Figure 4—figure supplement 3. FPA overexpression increases exonic proximal polyadenylation of RPP13.

Gene track showing proximal polyadenylation at the RPP13 gene locus, as detected with Illumina RNA-Seq, Helicos DRS, and Nanopore DRS.

Figure 4—figure supplement 4. FPA overexpression causes intron retention and exonic proximal polyadenylation at intron 3 of RPS4.

Gene track showing proximal polyadenylation at the RPS4 gene locus, as detected with Illumina RNA-Seq, Helicos DRS, and Nanopore DRS.