Table 3.
Leptosphaeria maculans | Plasmodiophora brassicae | |
---|---|---|
Genome size | 45.12 Mbp (Rouxel et al., 2011) | 25.5 Mbp (Schwelm et al., 2015) |
Feature of genome | AT-rich blocks containing effector genes and transposable elements, both of which is subjected to frequent repeat-induced point mutation (RIP) (Rouxel et al., 2011) | Low number of genes, low content of repetitive elements (Schwelm et al., 2015) |
Races/Isolates/Pathotypes identified and cloned (bold font has been cloned) |
*Pathogenicity groups (Koch et al., 1991; Mengistu et al., 1991) PG1- non aggressive isolate PG2- avirulent on “Quinta” and “Glacier” PG3 – virulent on susceptible check “Westar” and Glacier but avirulent on “Quinta” PG4 – virulent on all three cultivars *This PG classification was further reclassified based on different B. napus hosts (Badawy et al., 1991; Kutcher et al., 1993) AvrLm1 (Gout et al., 2006) AvrLm2 (Ghanbarnia et al., 2015) AvrLm3 (Plissonneau et al., 2016) AvrLm4-7 (Parlange et al., 2009) AvrLm5 later known as AvrLmJ1 (Van de Wouw et al., 2014; Plissonneau et al., 2017b) AvrLm6 (Fudal et al., 2007) AvrLm7 (Balesdent et al., 2002; Parlange et al., 2009) AvrLm8 (Balesdent et al., 2002) AvrLm9 (Balesdent et al., 2005) AvrLm10 (Petit et al., 2016) AvrLm11 (Balesdent et al., 2013) AvrLmS (Van de Wouw et al., 2009) AvrLepR1 (not genetically characterized) AvrLepR2 (not genetically characterized) AvrLepR3 (not genetically characterized) AvrLepR4 (not genetically characterized) |
Williams differential: Race 2, 3, 4, 5, 6, 7, 8 (Williams, 1966) European Clubroot Differential: Coding system based on differential set comprising five hosts each of B. campestris, B. napus and B. oleracea using 34 European P. brassicae collections (Buczacki et al., 1975) Somé differential (France population): Five pathotypes, P1, P2, P3, P4, and P5 (Somé et al., 1996) |
Affecting countries and prevalence of isolate pathotype/race found | Western Canada (2010–2011, Alberta, Saskatchewan, Manitoba): 674 isolates majority AvrLm2, 4, 6, 7, (S) (Liban et al., 2016) Germany (2011–2013): out of 644 isolates, majority of the tested isolates (85%) were virulent toward B. napus Rlm genes (Rlm1, 3, 4, 9). Rlm7 remains effective. Hence, the prevalent isolates harbor: AvrLm5, 6, 7, 8 (Winter and Koopmann, 2016) UK, Germany, Sweden, Poland (2002–2003) – 603 isolates genotyped, majority AvrLm5, 6, 7 (Stachowiak et al., 2006) France (2000-2001) −1797 isolates genotyped, majority AvrLm5, 6, 7, 8 (Balesdent et al., 2006) American continent (2004–2006): AvrLm1, 2, 4, 6, 7 (Dilmaghani et al., 2009) Australia (1987–2015): AvrLm1, 2, 3, 4, 5, 6, 7. Frequency of AvrLm1, 4 and 6 fluctuated across the years depending on which type of cultivar carrying specific R gene was commonly grown. Overall, AvrLm4 was extremely low compared to AvrLm1 and AvrLm6. Frequency of AvrLm3 was also low (Marcroft et al., 2012a; Van de Wouw et al., 2017) |
Canada (2005, Edmonton, Alberta): homogenous, ECD -/15/12 or Williams pathotype 3 or Somé P2 (Strelkov et al., 2007) Canada (2003, Alberta): ECD 16/15/12 and 16/15/0 or Williams pathotype 3 and 5 respectively; British Columbia ECD 16/2/12 or Williams pathotype 6; Ontario ECD 16/0/14 or Williams pathotype 6 (Strelkov et al., 2006) China: Williams race 4 (Chai et al., 2014) Czech Republic: Williams 7 most prevalent others include 6, 4, 9, 10, 2, 3, and 1 (Ríčarová et al., 2016) |
Resistance breakdown |
Rlm1 (within 5 years in France) (Rouxel et al., 2003a; Sprague et al., 2006) LepR3 (within 3 years in Australia) (Brun et al., 2000; Sprague et al., 2006), first sign of breakdown was detected within a year (Li et al., 2003) Rlm7 (France, 6 years after commercially released 2004–2010) (Mollier, 2015). Rlm6 (France) field trial experiment, breakdown after 3 years (Brun et al., 2010) Rlm3 (Canada) (Zhang et al., 2016a) |
“Mendel” succumbed from susceptible volunteers in Germany (Diederichsen et al., 2014) |
This PG classification etc.