Abstract Protein translation is tightly and precisely controlled by multiple mechanisms including upstream open reading frames (uORFs), but the origins of uORFs and their role in maize are largely unexplored. In this study, an active transposition event was identified during the propagation of maize inbred line B73. The transposon, which was named BTA for ‘B73 active transposable element hAT’, creates a novel dosage-dependent hypomorphic allele of the hexose transporter gene ZmSWEET4c through insertion within the coding sequence in the first exon, and results in reduced kernel size. The BTA insertion does not affect transcript abundance but reduces protein abundance of ZmSWEET4c, probably through the introduction of a uORF. Furthermore, the introduction of BTA sequence in the exon of other genes can regulate translation efficiency without affecting their mRNA levels. A transposon capture assay revealed 79 novel insertions for BTA and BTA-like elements. These insertion sites have typical euchromatin features, including low levels of DNA methylation and high levels of H3K27ac. A putative autonomous element that mobilizes BTA and BTA-like elements was identified. Together, our results suggest a transposon-based origin of uORFs and document a new role for transposable elements to influence protein abundance and phenotypic diversity by affecting the translation rate.
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Transgenic direct terminal repeats of Dissociation (Ds) produce chromosomal breakage in maize
Abstract Barbara McClintock recognized transposable elements originally by the movement of a site of chromosomal breakage, a genetic element calledDissociation(Ds) that was induced to break or transpose by another element she calledActivator. The chromosome breaking version, when analyzed on the molecular level was one transposon inside another. It is now known that transposition involving transposon termini in non-standard orientation with reference to each other results in chromosomal breakage. Here we used engineered transposon ends together with a phenotypic marker to cause targeted chromosomal breaks. The results indicate that engineered direct orientation of the naturally inverted repeats ofDissociationcan cause chromosomal breakage at the transgenic sites of insertion.
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- Award ID(s):
- 2214243
- PAR ID:
- 10472149
- Publisher / Repository:
- Springer Science + Business Media
- Date Published:
- Journal Name:
- The Nucleus
- Volume:
- 66
- Issue:
- 3
- ISSN:
- 0029-568X
- Format(s):
- Medium: X Size: p. 311-319
- Size(s):
- p. 311-319
- Sponsoring Org:
- National Science Foundation
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