Ganoderma, P.A.Karsten, 1881

Ho, C. - L. & Tan, Y. - C., 2015, Molecular defense response of oil palm to Ganoderma infection, Phytochemistry 114, pp. 168-177 : 169-170

2. Ganoderma spp. reported in BSR

The fruiting body of Ganoderma lucidum has gained wide popularity as a dietary supplement especially in China, Taiwan and, Japan for its perceived health benefits in preventing immunological diseases, such as hypertension and tumorigenesis ( Liu et al., 2002). Many Ganoderma species are also plant pathogens to khair, grapevines, betel palm, rubber, tea, and oil palm ( Turner, 1965; Bakshi et al., 1976; Adaskaveg and Gilbertson, 1987). G. lucidum was first reported as a causal agent of BSR in oil palm in 1930 ( Thompson, 1931; Utomo et al., 2005). Subsequently, six additional species were reported to be associated with BSR in Malaysia and Indonesia, including Ganoderma boninense, Ganoderma tornatum, Ganoderma chalceum, Ganoderma zonatum , and Ganoderma xylonoides ( Steyaert, 1967). To date, a total of 15 Ganoderma species have been detected in oil palms ( Turner, 1981). Although G. boninense was identified as the most virulent species that caused BSR, multiple species could be responsible for the disease on individual trees ( Ho and Nawawi, 1985).

2.1. Life cycle of Ganoderma spp. and its relation to BSR

Ganoderma spp. are classified as basidiomycetes. The life cycle of G. boninense in relation to BSR has been studied by Hasan and Flood (2003). Generally, each basidiospore germinates into a genetically unique monokaryotic hypha which is saprophytic and able to colonize dead palm wood. Ganoderma spp. have a tetrapolar mating system which favors outcrossing. They are heterothallic with two pairs of alleles at two mating loci, thus ensuring maximum genetic diversity by restricting inbreeding to 25% ( Rees et al., 2009). Hyphae of compatible mating type anastomose to produce a dikaryotic mycelium which could be potentially invasive. This heterokaryon proliferates and grows, with two haploid nuclei dividing and multiplying independently in each septated unit until the life cycle of Ganoderma is completed when the dikaryotic hyphae produce a fruiting body known as a basidiocarp ( Hasan and Flood, 2003). The basidiocarp bears specialized cells called basidia which resemble little clubs where karyogamy occurs. The basidia then divide meiotically to produce genetically unique basidiospores ( Campbell et al., 2008).

2.2. Transmission of BSR

Various sources of infection and modes of transmission, have been proposed for BSR. Basidiospores have been proposed as a source of BSR infection ( Pilotti et al., 2003; Rees et al., 2012). Basidiocarps are able to release a high number of basidiospores which can travel a long distance ( Sanderson, 2005) and become a source of infection for a wounded palm surface created during plantation harvesting and management ( Rees et al., 2012). Anastomosis of basidiospore germlings could occur on palm surface, debris or fallen palms in soil causing direct infection via cut fronds or indirect infection through roots ( Rees et al., 2012). Spread through basidiospores must be accountable for from the genetic diversity of Ganoderma isolates from the field ( Miller et al., 1999; Pilotti et al., 2003). Root invasion was considered as the primary route of transmission of BSR ( Rees et al., 2009). Since Ganoderma spp. have poor competitive saprophytic capability in soil, colonized debris left in the field by infested palms from previous planting of coconut or oil palm have been proposed as a very important source that provides the substantial amount of inocula required for root infection ( Hasan and Turner, 1998; Rees et al., 2007). The infection of oil palm is likely to occur when the roots come into contact with inocula from the debris left in the ground ( Flood et al., 2005), or from roots of neighboring infected palms.

The tetrapolar heterothallism of Ganoderma spp. also explains a number of phenomena:

1. Genetic diversity of isolates within a plantation was as great as between plantations whereby the vast genetic diversity of fungi observed on the infected palms could be a result of plasmogamy of genetically different mycelia derived from basidiospores;

2. BSR takes a long time to be evident in the field due to the requirement of plasmogamy or anastomosis of compatible mating types to form virulent dikaryotic mycelium, and they have weak competitive ability in soil or on organic debris ( Rees et al., 2007);

3. BSR symptoms may not be detectable even though Ganoderma spp. can be detected on palms whereby the fungus could be in the form of monokaryotic mycelia living saprophytically on dead tissues on the palm surface since monokaryotic mycelium are non-infective ( Goh, 2005; Rees et al., 2007).

2.3. Development and progress of BSR in oil palm roots

The development and progress of BSR in oil palm roots have been studied by Rees et al. (2009) in great detail. Briefly, infection by Ganoderma spp. is initiated by the penetration of oil palm root surface (epidermis and exodermis) by fungal mycelia, followed by a longitudinal progression of hyphae through inner and thin-walled cortex, and colonization of the lower stem (bole) eventually. Host cells in newly colonized tissue were shown to be colonized by intracellular hyphae and contained intact cell wall, intact cytoplasm, and organelles ( Rees et al., 2009). At this stage, depletion of starch grains in the cytoplasm was observed in host cells in advance of invasion and in the lower stem of infected oil palm ( Rees et al., 2009). Ganoderma spp. may behave as hemi-biotrophs in newly colonized tissues before turning into necrotrophic pathogens as implicated by extensive degradation of host cell walls. Cell wall degrading enzymes (CWDEs) such as cellulase, manganese peroxidases and laccases that are involved in the degradation of cellulose and lignins, are expected to be released by the fungus. At this stage, the host cells were colonized by hyphae intra-, intercellularly and intramurally. Rees et al. (2009) also suggested that the defense response of oil palm may rely on production and release of antimicrobial compounds rather than on cell wall strengthening. In the subsequent stage, the oil palm roots are surrounded by a tough and melanised mycelium (pseudo-sclerotium) with thin-walled hyphae encased by many thick-walled cells ( Rees et al., 2009). This leads to massive hyphal aggregations outside the oil palm roots, culminating in the formation of basidiocarps and release of basidiospores ( Rees et al., 2009). An infected oil palm tree may or may not bear any fruiting bodies. The presence of a fruiting body on an infected palm normally shows that the fungus has been in the wood for at least several years, and an extensive decay could have taken place in the stem ( Najmie et al., 2011).