Vegetative compatibility and genetic analysis of Colletotrichum lindemuthianum isolates from Brazil

Abstract

ABSTRACT. The causal agent of common bean anthracnose, Colletotrichum lindemuthianum, has considerable genetic and pathogenic variability, which makes the development of resistant cultivars difficult. We examined variability within and between Brazilian pathotypes of C. lindemuthianum through the identification of vegetative compatibility groups (VCGs) and by RAPD analysis. Two hundred and ninety-five nit mutants were obtained from 47 isolates of various pathotypes of the fungus collected from different regions, host cultivars and years. In complementation tests, 45 VCGs were identified. Eighteen RAPD primers were employed in the molecular analyses, producing 111 polymorphic bands. Estimates of genetic similarities, determined from the Sorence-Dice coefficient, ranged from 0.42 to 0.97; the dendrogram obtained by cluster analysis revealed 18 groups of isolates. RAPD and VCG markers presented high genotypic diversity. The number of significant associations (P = 0.05) between RAPD, VCG and pathogenicity markers ranged from 0 (VCG) to 80% (pathogenicity). The test of multilocus association (r d ) for RAPD markers was significantly different from zero (P < 0.001), suggesting linkage disequilibrium. However, the results for VCG markers show the presence of recombination mechanisms. In conclusion, RAPD markers and VCGs were useful for detecting genetic variability among isolates of C. lindemuthianum. We found considerable diversity among isolates from the same geographic origin within a short interval; this suggests rapid evolution. There is a need for further studies to elucidate the population structure of this pathogen in agro-ecosystems.

Heterokaryon Incompatibility Is Suppressed Following Conidial Anastomosis Tube Fusion in a Fungal Plant Pathogen

“…Thus, although the development of vegetative heterokaryotic cells may be advantageous for filamentous fungi, the genetic mechanism of vegetative incompatibility may also restrict the process between two genetically different individuals. It has recently been shown that genetic diversity in natural populations of C. lindemuthianum is considerable and that numerous vegetative compatibility groups are present [14]. However, our knowledge of vegetative incompatibility in Colletotrichum species is still very limited [7], [14].…”

Anastomosis groups and molecular variation in Pseudocercospora griseola

“…It was not possible to prove the parasexual cycle in this study, which requires auxotrophic mutants as described for other species (Stromnaes and Garber, 1963;Castro-Prado et al, 2007;Milgroom et al, 2009;Barcelos et al, 2011). Other tools have recently been used such as nucleus-targeting fluorescent proteins and insertion of hygromycin-and phleomycin-resistance genes.…”

“…Genetically different isolates of C. lindemuthianum showed the capacity for hyphal anastomosis between one another, which could contribute to increased genetic variability (Ishikawa et al, 2008). However, studies using nit mutants showed a predominance of vegetative incompatibility in C. lindemuthianum (Castro-Prado et al, 2007;Barcelos et al, 2011), and despite anastomosis formation, vegetative incompatibility reaction occurs afterwards, leading to cell death (Ishikawa et al, 2012).…”

PacCl, a pH-responsive transcriptional regulator, is essential in the pathogenicity of Colletotrichum lindemuthianum, a causal agent of anthracnose in bean plants

“…The use of phytopathogen-resistant cultivars is the main strategy to contain this disease in Brazil (Damasceno e Silva et al 2007). However, due to the large genetic variability of C. lindemuthianum, the breakdown of resistance prevents the use of cultivars for long periods of time, thus hindering the establishment of a permanent solution to the disease (Rodriguez-Guera et al 2003;Ansari et al 2004;Mahuku and Riascos 2004;Barcellos et al 2011). The large genetic and pathogenic variability found in Colletotrichum species has been extensively studied, and it can be partially explained by recombinant events and mutations caused by the presence of transposons (Casela and Frederiksen 1994;Santos et al 2012), and by the presence of anastomoses among conidia (Roca et al 2003;Castro-Prado et al 2007;Rosada et al 2010;Franco et al 2011).…”