Agriculture Reference
In-Depth Information
(Schafer, 1971). Moreover, the differences in response can be large. For example, the yield
loss of wheat cultivars under a comparable severity of rust infection ranged from 9.5%
to 44.5% (cited by Schafer, 1971). So why, given potential benefi ts of this scale, is toler-
ance still so poorly understood? There are several factors that may have contributed to the
disappointing progress to date including a lack of consensus on how tolerance should be
defi ned, practical diffi culties in quantifying it, and its apparent low heritability.
The term tolerance has been used widely and inconsistently in the literature and for
a number of years this hindered the development of a clear conceptual framework for
research into the physiological mechanisms underlying tolerance (Gaunt, 1981; Clarke,
1984). Some authors have used the term tolerance to describe partial or incomplete
resistance to infection. In this context, 'tolerant' genotypes are distinguished from less
'tolerant' types by exhibiting a lower severity of infection. More commonly, tolerance has
been defi ned in terms of the ability to maintain an acceptable seed yield, or some other
measure of plant fi tness or productivity, under a given severity of pathogen infection,
thus distinguishing it from resistance (Caldwell
et al.
, 1958; Schafer, 1971). A further
distinction has been made between tolerance of the pathogen and tolerance of disease
(Gaunt, 1981; Clarke, 1984; Newton
et al.
, 1998; Inglese & Paul, 2006). According to
Inglese & Paul (2006) tolerance of infection is the relationship between the presence
of the pathogen and disruption of normal host physiology, whereas tolerance of dis-
ease is the relationship between host growth or fi tness and the physiological disruption
resulting from infection. For example, the native rust fungus
Coleosporium tussilginis
resulted in smaller reductions in net CO
2
fi xation of
Senecio vulgaris
per unit of infection
than the alien rust
Puccinia lagenophorae
indicating a greater level of pathogen tolerance
in the
S. vulgaris
-
C
.
tussilginis
interaction. By contrast there was no difference between
the two pathosystems in the reduction in host growth and fi tness per unit reduction in photo-
synthesis, indicating that tolerance of disease in each case was comparable (Inglese &
Paul, 2006).
However, attempting to distinguish between tolerance of the pathogen and tolerance
of disease can be potentially misleading, because it usually requires singling out specifi c
processes by which to measure physiological dysfunction. In reality, the overall effect
of the pathogen on growth and yield will be the net outcome of numerous physiologi-
cal adjustments stemming from the primary disruption to the tissue. In practice, it can
also be diffi cult to distinguish unequivocally between measures of infection severity and
symptoms of disease. For example, to what extent should necrotic tissue within a lesion
be considered a measure of pathogen presence or leaf damage and physiological dysfunc-
tion? Some authors have suggested that the term tolerance of disease is meaningless or
unnecessary and that all tolerance is in reality tolerance of the pathogen (Parbery, 1978;
Gaunt, 1981). According to Parbery (1978), if tolerance of the pathogen is defi ned as
the capacity of the host to support pathogen growth with little disturbance to the host
metabolism, then complete pathogen tolerance implies no disease. Indeed it is diffi cult
to envisage the converse situation where tolerance of the pathogen may be low (implying
signifi cant disruption to host physiology), but tolerance of disease high (little effect on
growth and yield), unless the disruption is highly localised and the plant as a whole can
compensate for the impaired function. There are examples of this in the insect herbivory
literature where damage to apical meristems can lead to the outgrowth of axillary buds
(Tiffi n, 2000), but little evidence that it occurs in response to pathogen infection.
