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Plant genetic archaeology: whole-genome sequencing reveals the pedigree of a classical trisomic line.

Salomé PA, Weigel D - G3 (Bethesda) (2014)

Bottom Line: The circadian oscillator is astonishingly robust to changes in the environment but also to genomic changes that alter the copy number of its components through genome duplication, gene duplication, and homeologous gene loss.While studying the potential effect of aneuploidy on the Arabidopsis thaliana circadian clock, we discovered that a line thought to be trisomic for chromosome 3 also bears the gi-1 mutation, resulting in a short period and late flowering.With the help of whole-genome sequencing, we uncovered the unexpected complexity of this trisomic stock's history, as its genome shows evidence of past outcrossing with another A. thaliana accession.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, Max Planck Institute for Developmental Biology, D-72076 Tübingen, Germany salome@chem.ucla.edu.

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Possible models to explain the genesis of CS3227. In models (A) and (B), the complement of primary trisomics was generated from a cross between a diploid and a tetraploid Col-1 parent. The nonequal segregation of chromosomes in the F1s was induced by X-ray irradiation, which may have caused the gi-1 deletion (A). Alternatively, gi-1 may have been the diploid parent (B). The introduction of the Est-like genome occurred after the isolation of trisomic individuals, either by targeted crossing or by outcrossing to a neighboring Est-like plant. In model (C), two diploid parents, Col-1 and Est-like, were crossed and the F1 plants X-ray irradiated. The extent of Est-like genome was subsequently largely lost following backcrosses to Col-1 or by single-seed decent. As in (A), model (C) posits the genesis of gi-1 as a consequence of X-ray irradiation of the F1 generation.
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fig8: Possible models to explain the genesis of CS3227. In models (A) and (B), the complement of primary trisomics was generated from a cross between a diploid and a tetraploid Col-1 parent. The nonequal segregation of chromosomes in the F1s was induced by X-ray irradiation, which may have caused the gi-1 deletion (A). Alternatively, gi-1 may have been the diploid parent (B). The introduction of the Est-like genome occurred after the isolation of trisomic individuals, either by targeted crossing or by outcrossing to a neighboring Est-like plant. In model (C), two diploid parents, Col-1 and Est-like, were crossed and the F1 plants X-ray irradiated. The extent of Est-like genome was subsequently largely lost following backcrosses to Col-1 or by single-seed decent. As in (A), model (C) posits the genesis of gi-1 as a consequence of X-ray irradiation of the F1 generation.

Mentions: Even with full genome sequence from our CS3227 stock, it is difficult to reconstruct the exact chain of events that led to its genesis. Three major events must have taken place, the order of which is not clear: the isolation of a trisomic stock for chromosome 3; the introduction of the gi-1 deletion; and the introgression of an Est-like genome. Trisomic lines for other chromosomes do not share the gi-1 deletion (not shown), arguing against the model depicted in Figure 8B, in which the gi-1 mutant was used as diploid parent in the original diploid x tetraploid cross. gi-1 and the trisomic lines were both generated by irradiating A. thaliana with X rays (Redeí 1962; Steinitz-Sears 1963); it is therefore conceivable that gi-1 was isolated in the progeny of the diploid x tetraploid cross (Figure 8, A and C). Although we favor this scenario, we notice that gi-1 and CS3227 do not share more SNPs with each other than with gi-2. However, ionizing agents do not induce as many point mutations as EMS (Belfield et al. 2012) and may therefore not live an easily trackable footprint.


Plant genetic archaeology: whole-genome sequencing reveals the pedigree of a classical trisomic line.

Salomé PA, Weigel D - G3 (Bethesda) (2014)

Possible models to explain the genesis of CS3227. In models (A) and (B), the complement of primary trisomics was generated from a cross between a diploid and a tetraploid Col-1 parent. The nonequal segregation of chromosomes in the F1s was induced by X-ray irradiation, which may have caused the gi-1 deletion (A). Alternatively, gi-1 may have been the diploid parent (B). The introduction of the Est-like genome occurred after the isolation of trisomic individuals, either by targeted crossing or by outcrossing to a neighboring Est-like plant. In model (C), two diploid parents, Col-1 and Est-like, were crossed and the F1 plants X-ray irradiated. The extent of Est-like genome was subsequently largely lost following backcrosses to Col-1 or by single-seed decent. As in (A), model (C) posits the genesis of gi-1 as a consequence of X-ray irradiation of the F1 generation.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4321033&req=5

fig8: Possible models to explain the genesis of CS3227. In models (A) and (B), the complement of primary trisomics was generated from a cross between a diploid and a tetraploid Col-1 parent. The nonequal segregation of chromosomes in the F1s was induced by X-ray irradiation, which may have caused the gi-1 deletion (A). Alternatively, gi-1 may have been the diploid parent (B). The introduction of the Est-like genome occurred after the isolation of trisomic individuals, either by targeted crossing or by outcrossing to a neighboring Est-like plant. In model (C), two diploid parents, Col-1 and Est-like, were crossed and the F1 plants X-ray irradiated. The extent of Est-like genome was subsequently largely lost following backcrosses to Col-1 or by single-seed decent. As in (A), model (C) posits the genesis of gi-1 as a consequence of X-ray irradiation of the F1 generation.
Mentions: Even with full genome sequence from our CS3227 stock, it is difficult to reconstruct the exact chain of events that led to its genesis. Three major events must have taken place, the order of which is not clear: the isolation of a trisomic stock for chromosome 3; the introduction of the gi-1 deletion; and the introgression of an Est-like genome. Trisomic lines for other chromosomes do not share the gi-1 deletion (not shown), arguing against the model depicted in Figure 8B, in which the gi-1 mutant was used as diploid parent in the original diploid x tetraploid cross. gi-1 and the trisomic lines were both generated by irradiating A. thaliana with X rays (Redeí 1962; Steinitz-Sears 1963); it is therefore conceivable that gi-1 was isolated in the progeny of the diploid x tetraploid cross (Figure 8, A and C). Although we favor this scenario, we notice that gi-1 and CS3227 do not share more SNPs with each other than with gi-2. However, ionizing agents do not induce as many point mutations as EMS (Belfield et al. 2012) and may therefore not live an easily trackable footprint.

Bottom Line: The circadian oscillator is astonishingly robust to changes in the environment but also to genomic changes that alter the copy number of its components through genome duplication, gene duplication, and homeologous gene loss.While studying the potential effect of aneuploidy on the Arabidopsis thaliana circadian clock, we discovered that a line thought to be trisomic for chromosome 3 also bears the gi-1 mutation, resulting in a short period and late flowering.With the help of whole-genome sequencing, we uncovered the unexpected complexity of this trisomic stock's history, as its genome shows evidence of past outcrossing with another A. thaliana accession.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, Max Planck Institute for Developmental Biology, D-72076 Tübingen, Germany salome@chem.ucla.edu.

Show MeSH
Related in: MedlinePlus