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Introduction to Fungi, Third Edition

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GLOMERELLACEAE<br />

389<br />

infection process stalls. Infection is continued on<br />

the ripened fruits after a period of s<strong>to</strong>rage.<br />

This infection strategy enables the pathogen <strong>to</strong><br />

avoid the high levels of phy<strong>to</strong>alexins in unripe<br />

fruits (Latunde-Dada, 2001). Resumption of development<br />

is triggered by the strong increase in<br />

ethylene levels associated with fruit ripening<br />

(Flaishman & Kolattukudy, 1994).<br />

Endophytic colonization<br />

Several anthracnose pathogens including<br />

C. musae, C. coccodes and strains of C. gloeosporioides<br />

develop a prolonged latent phase inside their<br />

host plant (Rodriguez & Redman, 1997).<br />

Colonization during the endophytic phase may<br />

begin by infection through s<strong>to</strong>mata rather than<br />

direct penetration of the epidermis, and intercellular<br />

colonization of host tissue. During<br />

senescence of the host plant, the host’s<br />

immune system degenerates and active colonization<br />

may ensue, resulting in the development of<br />

sporulating anthracnose-type lesions. Freeman<br />

and Rodriguez (1993) and Redman et al. (1999a)<br />

have shown that the deletion of a single gene<br />

can convert an aggressive pathogen (C. magna)<br />

<strong>to</strong> a permanently symp<strong>to</strong>mless endophyte.<br />

This finding emphasizes the possibility that<br />

‘endophytic mutualism is only a gene away<br />

from pathogenicity’ (Latunde-Dada, 2001), and<br />

also indicates one mechanism by which endophytes<br />

may evolve in nature. A further fundamental<br />

point of interest is that colonization by<br />

such symp<strong>to</strong>mless endophytes renders the host<br />

plant resistant against infection by pathogenic<br />

strains of the same species, and also other fungal<br />

pathogens (Redman et al., 1999b).

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