Research ArticleGENETICS

Genome elimination mediated by gene expression from a selfish chromosome

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Science Advances  03 Apr 2020:
Vol. 6, no. 14, eaaz9808
DOI: 10.1126/sciadv.aaz9808
  • Fig. 1 Composition and origin of PSR chromosome.

    (A) Circular portrayal of the PSR chromosome scaffolds. The scaffolds are organized from largest to smallest (their natural order with respect to each other could not be determined with current data). The outermost track represents repetitive satellites with outer bars representing the positive DNA strand, and the inner bars represent the negative DNA strand. The colors represent the four major (70.32%) satellite families. The middle track represents other repetitive sequences (17.89%) including TEs, low-complexity regions, and telomeric sequences. The innermost track represents protein coding sequences (8.57%), and the color ranges from black to red for low to high expression, respectively. (B) The relationship of NV79 repeats between PSR scaffolds and host chromosomes 1 to 5, indicating that PSR repeats are homologous to sequences found on all chromosomes. (C) The relationship of PSR protein scaffolds sequences and host chromosomes. The links are colored by blast bit scores from red (highest) to blue (lowest). (D) Heat map of PSR gene with expression values higher than 10 TPM (table S8, columns M to Q). Expression levels are portrayed in colors ranging from white (low to no expression) to blue (highest expression). PSR genes that were disrupted with RNAi in this study are shown in red.

  • Fig. 2 Effects of haploidizer targeted by RNAi in early embryos.

    (A) Efficiency of RNAi measured by relative gene expression of the targeted genes. Asterisks indicate significant expression differences between control and RNAi-treated individuals [n = 5, P < 0.05, one-way analysis of variance (ANOVA) with Tukey’s multiple comparisons test]. (B) Proportion of G1 females was measured for control and RNAi-treated wasps. The box plots depict the median (thick horizontal line within the box), the 25th and 75th percentiles (box margins), and the 1.5 interquartile range (thin horizontal line). (C) Confocal imaging of sperm from WT, PSR+, and haploidizer RNAi-treated PSR+ males. (D) Nuclei of individual embryos from WT, PSR+, and haploidizer RNAi-treated PSR+ fathers, stained for PSR (red) and rDNA (green). (E) Nuclei from individual embryos from WT, PSR+, and haploidizer RNAi-treated PSR+ fathers, stained for the histone marks, H3K9me2,3 (top panels, red), and H4K20me1 (bottom panels, also red). DNA is blue in all panels. PCM, paternal chromatin mass; 2N, diploid nuclei; N, haploid nuclei.

  • Fig. 3 Genetics and active model of PSR-induced genome elimination.

    (A) The effects of RNAi knockdown of haploidizer on PSR transmission and the proportion of female offspring. The pie charts indicate the proportion of males (gray) and females (purple). (B) Model for involvement of haploidizer in PGE. Expression of PSR’s haploidizer gene leads to failure of the paternal chromatin to resolve into chromosomes. This action inhibits the activation of female transformer (traF) and, thus, female development. As a result, these fertilized eggs develop into haploid male offspring that carry PSR. RNAi treatment of haploidizer mitigates the chromatin defects, allowing partial expression of traF from the paternal set. This action reestablishes the female developmental pathway.

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