Gene family size distributions were fit to power laws to compare gene duplication trends in pathogens versus non-pathogens.
Although there are numerous examples of gene family expansion in pathogenic lineages of fungi [ 10, 22, 24, 26, 29, 31, 38, 53], to date, gene duplication trends across whole genomes have not been analyzed.
In particular, Lhcb1 appears to have been particularly prone to the accumulation of recent gene duplications, a trend that seems to have also occurred in Arabidopsis and poplar.
Although non-WGD paralogous pairs have different times of duplication, the overall trend shows that WGD pairs have much greater paralog sequence identity, which could mean that either the mutation rate r is smaller for WGD pairs than for non-WGD pairs, or that many of the individual small-scale duplication events are more recent than the WGD event.
To compare redundancy trends by duplication origin, gene pairs were labeled according to previous genome-wide analyses that identified recent segmental duplication events in Arabidopsis [ 32] as well as tandem and single duplications [ 33].
Gene family expansion in species with overall higher levels of duplication also showed functional trends that could be reconciled with organismal life histories [ 9- 15, 18, 18, 36, 37, 55, 60, 66, 75].
In stark contrast, very different functional trends characterised duplications younger than 2R, corresponding to tandem or segmental duplications (mapped to 5,495 unique human Entrez Genes).
Intra-chromosomal duplicates in zebrafish and medaka had intermediate Ks values between tandem and inter-chromosomal duplication with an upward trend correlated with increasing duplication set size.
Although the nature of the assay did not allow us to handle large number of cells, at least ten SPBs were analyzed for each time point to capture a trend for duplication timing.
This indicates that the GSTs in the Delta and Epsilon subclasses have a greater general trend of duplication than the GSTs in the other four subclasses as previously reported by Friedman [ 30].> -wrap-foot>> -wraTheoot> aThe gene IDs were obtained directly from the published DBM genomic database (DBM-DB: http://iae.fafu.edu.cn/DBM/family/PxGSTs.php).fafu.edu.cn/DBM/family/PxGSTs.php
The chromosomal distribution of SV events were further examined to reveal distinct trends for segmental duplications vs. deletions.
