The model considers the probability of duplicate packet generations.
The duplication degeneration complementation model of gene duplication (Force et al. 1999) predicts that degenerative mutations in regulatory elements can increase (rather than reduce) the probability of duplicate gene preservation and predicts that the usual mechanism of duplicate gene preservation is the partitioning of ancestral functions rather than the evolution of new functions.
According to the duplication-degeneration-complementation (DDC) model [35] degenerative mutations in regulatory elements can increase the probability of duplicate gene preservation and the mechanism of preservation of duplicate genes is partitioning of ancestral functions.
To reduce the probability of duplicate sampling, sampled individuals were separated by a minimum of 10 m.
It has also been proposed that one of the factors influencing the probability of duplicate gene retention is its connectivity [ 22].
In the case of P. trichocarpa, the negative degree centrality coefficient leads to an inverse relationship between connectivity and the probability of duplicate retention in the presence of few duplicated neighbors.
To what degree do different genetic variables in a diploid species influence the probability of duplicate gene persistence in a closely related species after WGD? Table 1 presents the results of logistic regression between 10 variables in the diploid species S. tropicalis on the outcome of duplicate gene persistence in the tetraploid species X. laevis.
Although probabilities of duplicates acquiring novel and beneficial functions is lower than duplicates being silenced [ 3], the classical model of the fates of duplicate genes proposed by Ohno is coming under increasing scrutiny [ 4- 6].
Here, we have shown that the topological properties of ENTS-predicted networks, including the first whole-genome interactome for P. trichocarpa, are related to the probability of WGD duplicate gene retention following independent duplication events in a manner consistent with the predictions of the gene balance hypothesis.
Without genetic buffering, we assume that the probability of a duplicate remains nonessential, that is, functionally compensated by another duplicate copy in the same genome, and decayed exponentially with the time t (the age of gene duplication), that is, e− λt, where λ is the loss rate of duplicate compensation by mutations.
