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Review
. 2005 Jan;17(1):4-11.
doi: 10.1105/tpc.104.170130.

Paralogs in polyploids: one for all and all for one?

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Free PMC article
Review

Paralogs in polyploids: one for all and all for one?

Reiner A Veitia. Plant Cell. 2005 Jan.
Free PMC article
No abstract available

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Figures

Figure 1.
Figure 1.
Dominant Negative Effects and Retention of Paralogs. (A) Punnett square showing all possible combinations of dimers produced from three normal A alleles and one mutant allele A′ that renders the dimer inactive. The presence of only one mutant allele out of four leads to 56% of normal dimer AA. (B) Passage through a reduced ploidy phase is even worse because only 25% of dimers will be active. This fraction corresponds, in genetic terms, to the proportion of homozygotes AA, which are favored by selection. Removal of the deleterious A′ allele from the population can be extremely effective during this phase if fitness depends tightly on AA. Similar results are obtained for the trimer A-B-A.
Figure 2.
Figure 2.
Dosage Effects and Retention of Paralogs. (A) In the context of the homodimer AA, consider that the synthesis of A results from the translation of the mRNA(A), present at a stable concentration, then A undergoes reversible dimerization or is degraded with a rate proportional to the concentration of monomers. According to this scheme, the concentration of AA in the steady state (ss) is proportional to the square of the ratio of specific rates of synthesis of A (Sa) and its degradation (Da; derivation in Veitia, 2004). Deletion of one allele out of four leads to 56% of normal AA. The graph shows the effects of deleting one, two, or three alleles expressed as the percentage of active AA with respect to the normal tetraploid system (the dotted line represents 50% of concentration of dimer). In a diploid phase, obliteration of one copy of A leads to 25% AA. Results are different if, for instance, AA becomes the degradable entity, as in a fast irreversible dimerization. When AA is degraded with a rate proportional to its concentration, a change in monomer input will have a proportional impact on the concentration of the dimer. (B) What happens to the trimer A-B-A in the steady state? Under similar assumptions as above, the yield of ABA depends again on the square of Sa. The black bars in the graph show the steady state amounts of ABA for different doses of the wild-type A allele (for the maximum/tetraploid dose of B). The gray bars show how deleting one allele of B increases dosage sensitivity of A. Again, the results are slightly different if the dimers or trimer are allowed to be degraded, and less dramatic effects are obtained when ABA is the only degradable entity.
Figure 3.
Figure 3.
Potential Impact of Allopolyploidization or Hybridization on Transcription. (A) Effect of an allopolyploidization event involving the two parental cells P1 and P2 on transcription from homologous promoters responding to the transactivator A. The black triangles represent the binding sites for A. (B) In the simplest case, the parental cells have similar volumes (Vol) and similar DNA contents but might contain different amounts of A and promoters with different thresholds (AThr). After the merger, let us suppose that the volume doubles and that the regulation of the expression of A is unaltered. It is easy to see that, in this particular case, the expected concentration of A is intermediate. For instance, this concentration can be suitable to trigger expression from the promoter coming from P1 but not from P2. (C) Transcriptional responses from promoters with three or four binding sites allowing cooperative interactions with the transactivator A. The solid curves are redrawn from Figure 5 of Veitia (2003b), with the same parameters. Decreasing the number of similar binding sites (n) shifts the position of the threshold to higher concentrations of A. In the case of a newly formed allopolyploid, if the resulting concentration of A is higher than the thresholds of both types of promoters (case A1), transcription is expected from both. If, on the contrary, the concentration of A is not high enough (i.e., A2), the red promoter will be on, while the green one will be off. Of course, cases of incomplete silencing are expected depending on the actual A concentration with respect to AThr. The thin black sigmoid represents a promoter with four binding sites that produces a response similar to that with three binding sites. It can be shown that there is an infinity of ways to obtain such a result, simply by changing the strength of the interaction between A and its binding sites, as long as cooperativity is maintained. This can explain the outcome of compensatory mutations.

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