Phenotypic diversification by gene silencing inPhytophthoraplant pathogens

Abstract

Advances in genome sequencing technologies have enabled generation of unprecedented information on genome content and organization. Eukaryote genomes in particular may contain large populations of transposable elements (TEs) and other repeated sequences. Active TEs can result in insertional mutations, altered transcription levels and ectopic recombination of DNA. The genome of the oomycete plant pathogen, Phytophthora infestans, contains vast numbers of TE sequences. There are also hundreds of predicted disease-promoting effector proteins, predominantly located in TE-rich genomic regions. Expansion of effector gene families is also a genomic signature of related oomycetes such as P. sojae. Deep sequencing of small RNAs (sRNAs) from P. infestans has identified sRNAs derived from all families of transposons, highlighting the importance of RNA silencing for maintaining these genomic invaders in an inactive form. Small RNAs were also identified from specific effector encoding genes, possibly leading to RNA silencing of these genes and variation in pathogenicity and virulence toward plant resistance genes. Similar findings have also recently been made for the distantly related species, P. sojae. Small RNA “hotspots” originating from arrays of amplified gene sequences, or from genes displaying overlapping antisense transcription, were also identified in P. infestans. These findings suggest a major role for RNA silencing processes in the adaptability and diversification of these economically important plant pathogens. Here we review the latest progress and understanding of gene silencing in oomycetes with emphasis on transposable elements and sRNA-associated events.

R/Avr gene expression study of Rpi-vnt1.1 transgenic potato resistant to the Phytophthora infestans clonal lineage EC-1

“…Across all these studies, including ours, Avrvnt1 gene expression has been very low in the virulent isolates and no clear evidence exists yet as to whether its detection in potato plants without the Rpi-vnt1.1 or Rpiphu1 genes reflect a real change in expression. Oomycete pathogens can evade recognition by silencing Avr gene which could be the explanation of the EC-1 virulence (Qutob et al 2009(Qutob et al , 2013Vetukuri et al 2013;Na et al 2014). Sub-clonal variation in virulence is typical for P. infestans such that isolates belonging to the same clonal lineage have different virulence patterns.…”

“…Gain of virulence resulting from Avr gene transcript differences has been described for the Avr2 and Avr-vnt1 genes in P. infestans (Gilroy et al 2011;Pel 2010). Gene silencing of effector genes to gain virulence is found in other oomycete pathogens such as Phytophthora sojae (Qutob et al 2009(Qutob et al , 2013Vetukuri et al 2013;Na et al 2014).…”

An epigenetic toolkit allows for diverse genome architectures in eukaryotes

“…This division of function within the P. infestans genome behaves almost as two functionally and spatially distinct genomes, and is determined by epigenetic mechanisms. RNAi-mediated heterochromatin formation not only controls the activity of mobile elements but also has major impacts on the transcription of nearby effector genes (more than half of all effector genes in P. infestans are within <2kb of a TE) where increasing proximity can alter an effector gene’s transcription due to the spreading of heterochromatin from targeted loci [91,92]. The combination of complex epigenetic silencing and the evolutionary impacts of the repetitive genome on gene evolution (e.g.…”

Evolutionary origins and impacts of genome architecture in ciliates

“…[1][2][3][4][5][6] While TEs are often described as parasitic or selfish DNA that are assumed to proliferate at the expense of the host genome's fitness (i.e., by increasing genome instability), 7,8 they remain essential and well-regulated genomic components, for example, possessing roles as centromeres and/or telomeres in Dictyostelium discoideum and Drosophila melanogaster, respectively. 9,10 Maintaining some control over genome instability provides massive fitness benefits to the host genome/organism, and is linked to genome dynamism, [11][12][13][14][15][16][17] which is exaggerated and well studied in pathogenic lineages (Phytophthora infestans and Entamoeba histolytica). [11][12][13] A dramatic example is the separation of germ-line and somatic genomes, which provides the means to protect the heritable genome while reaping the benefits of a highly dynamic and responsive soma.…”