252 P. BISWAS ET AL.
at 18◦C. However, 1-MCP resulted in increased decay susceptibility in
mature-green tomatoes stored at 3◦C (Jing and Zi-Sheng 2011) or at 2.5◦C
(Biswas et al. 2014b). It appears that the efficacy of 1-MCP in reduc-
ing decay depends on whether the decay is associated with ripening
or is chilling induced. At chilling temperatures (2.5◦Cor3◦C), 1-MCP
treated tomatoes were unable to ripen potentially rendering fruit more
sensitive to chilling and thus resulting in enhanced decay susceptibil-
ity. In contrast, fruit treated with 1-MCP and maintained at 20◦Cwere
physiologically less mature and had less decay than controls, possibly
by arresting the advancement of ripening as susceptibility increases as
fruit ripen (Fallik et al. 1993; Prusky 1996). During chilling, 1-MCP may
have interfered with ethylene-induced resistance to decay in ripening
tomato fruit (Geeson et al. 1986; D ́ıaz et al. 2002), while at 20◦C, 1-MCP
maintained fruit in the more resistant unripe condition. It can, there-
fore, be suggested that 1-MCP treatment accelerates decay in chilled
fruit but reduces decay associated with normal ripening which may
explain previous contradictory results.
Chilling-induced cell wall disassembly may contribute to decay sus-
ceptibility in fruit by altering the structure or accessibility of cell wall
substrates to pathogen cell wall-degrading enzymes (Cantu et al. 2008).
Many saprophytic and plant pathogenic organisms secrete cell wall-
degrading enzymes that specifically target cell wall components so that
pathogens can penetrate the host and acquire nutrients from digested
wall material and cellular contents (Collmer and Keen 1986). Ripen-
ing impaired tomato mutants Nrornor showed reduced ripening-
associated softening and decreased susceptibility to pathogens (Lavy-
Meir et al. 1989; Kramer et al. 1992). However, cell wall disassembly
alone cannot explain pathogen susceptibility in tomato. Suppression of
the ripening-associated EXP gene,LeExp1, resulted in firmer fruit with
prolonged shelf life, but did not reduce susceptibility toBotrytisand
Alternariain tomato (Cantu et al. 2008). They suggested that simulta-
neous suppression of bothLePGandLeExp1expression is an important
determinant of the ripening-associated increase in decay susceptibility.
In summary, there are various mechanisms that resist pathogen attack.
A pathogen, when it finds suitable conditions for penetration and estab-
lishment within host tissues, will cause a disease only if it succeeds in
circumventing the protective barrier of the host (Barkai-Golan 2001).
Factors that help pathogens to defeat the host barrier include the ability
to produce cuticle- and cell wall-degrading enzymes or the production
of toxic compounds. By comparison, defense mechanisms of the host
also depend on the ability of the intact cuticle to provide a barrier to
fungal penetration, the ability to produce antimicrobial activities and