To gain insight into patterns of retention and loss of duplications within protein kinase families, inferred syntenic regions were mapped onto a phylogeny of 940 kinases and then linked to gene expression data, family gene annotations and loss-of-function phenotypes.
However, this analysis did display putative evidence for the loss of duplicate copies from past duplication events, inferred from the presence of multiple pseudogenized genomic loci.
For instance, could redundancy resulting from polyploidy destabilize the incipient differentiation of the two paralogs, NRPD2/E2-a and NRPD2/E2-b, or could the occasional loss of primary duplication be compensated for by secondary duplications resulting from polyploidy?
These observations are consistent with loss of the duplication due to unequal crossing-over, as discussed above.
Loss of the duplication to generate a single copy of the MSH2 locus was selected on medium containing 5-fluoroorotic acid [79].
The relevant processes include divergent sequence evolution, gain and loss of interactions, duplication of genes and the corresponding interactions, and gain and loss of genes.
The rate of loss of the duplication from M184 and the transformants was measured during growth in liquid medium in the absence of antibiotic.
The proportions of colonies retaining norfloxacin resistance at 0 and 12 h were compared to calculate the probability of loss of the duplication using the following equation.
The time-dependent model is then extended to the age-dependent model, which allows the gene loss rate dependent of duplication events.
However, several factors obscure analyses of old duplication events, such as the frequent loss of genes after duplication, gene conversion and unequal evolutionary rates of paralogs.
