Hervé Gaubert, Diego H. Sanchez, Hajk-Georg Drost and Jerzy Paszkowski
Genetics: October 1, 2017; vol. 207; no. 2: 813-821; https://doi.org/10.1534/genetics.117.300103
Abstract
Retrotransposons (RTs) can rapidly increase in copy number due to periodic bursts of transposition. Such bursts are mutagenic and thus potentially deleterious. However, certain transposition-induced gain-of-function or regulatory mutations may be of selective advantage. How an optimal balance between these opposing effects arises is not well characterized. Here, we studied transposition bursts of a heat-activated retrotransposon family in Arabidopsis. We recorded a high inter and intraplant variation in the number and chromosomal position of new insertions, which usually did not affect plant fertility and were equally well transmitted through male and female gametes, even though 90% of them were within active genes. We found that a highly heterogeneous distribution of these new retroelement copies result from a combination of two mechanisms, of which the first prevents multiple transposition bursts in a given somatic cell lineage that later contributes to differentiation of gametes, and the second restricts the regulatory influence of new insertions toward neighboring chromosomal DNA. As a whole, such regulatory characteristics of this family of RTs ensure its rapid but stepwise accumulation in plant populations experiencing transposition bursts accompanied by high diversity of chromosomal sites harboring new RT insertions.
See http://www.genetics.org/content/207/2/813?etoc
Figure 3: Heat-induced transcriptional activation of chromosomal regions adjacent to new Onsen insertions. Strand-specific RNAseq analysis of pooled nrpd1 progeny and plant 2L progeny (Table 1) subjected to heat stress (S0) or grown in control conditions (C0). The figure displays representative screen shots of genome browser. New Onsen insertions in plant 2L are depicted as yellow boxes, with arrows indicating the direction of insertion. (A) Insertion into a gene promoter in sense orientation in respect to the affected gene. (B) Insertion into coding region of a gene in sense orientation. (C) Insertion into a gene promoter in sense orientation (note transcriptional activation of the neighboring gene). (D) Insertion into coding region of a gene in antisense orientation. (E) Insertion into intergenic region. (F) Insertion between genes showing negligible transcriptional disturbance. Treatments and genotype given left to the chromosomal tracks; CDS track mark gene coding sequences, red features represent transcripts in left to right orientation, and blue features transcript from right to left.
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