PNL Volume 12 1980 RESEARCH REPORTS 29
Hampton, R. 0. US Dept. Agric, Oregon State Univ., Corvallis, OR USA
In early efforts to identify Pisum germplasm immune to pea seedborne
mosaic virus (PSbMV) (1), I noted considerable diversity in symptoms expressed
by the 1,326 Plant Introduction accessions inoculated with this virus. The
range of PSbMV-induced symptoms made possible the selection of Pisum differen-
tials for standardized comparisons of PSbMV-like viruses and strains. Nineteen
such differentials, each responding to PSbMV inoculation with specific symptoms,
were used recently for definitive comparisons among PSbMV strains first
reported in Czechoslovakia, Japan, the U.S.A., and the Netherlands between
1966 and 1970 (2).
Symptoms induced in these differentials by PSbMV ranged from very rapid
development (5 to 9 days after inoculation) of whole-plant necrosis on one
extreme to very slight leaf rolling and/or vein clearing on the other.
Symptoms induced in differentials of intermediate reactions consisted of plant
stunting, vein swelling, tendril kinking, and downward rolling of leaves,
most commonly reported for this virus. At least some plants of three dif-
ferentials were immune to PSbMV.
This range of symptoms poses some interesting genetic implications,
because it is generally accepted that immunity to PSbMV is conferred by a
single recessive gene pair, sbm (3). Such a range of responses to PSbMV
infection would therefore appear to result from modification of susceptibility
or sensitivity, by genetic and/or environmental means. Accumulated evidence
indicates that the genetic influence is significant. Accordingly, whole-plant
necrosis would presumably be caused by the action of modifier genes than
enhance sensitivity to the virus (decrease tolerance), whereas tendencies
toward infection without symptoms (4) would presumably be caused by modifiers
that reduce sensitivity (increase tolerance).
Because it appears that such a modifier-gene system exists in peas, it
may also be appropriate to discuss the implications of this phenomenon for
breeders. Specifically, there is a possibility that in efforts to develop
PSbMV-immune cultivars, breeders might mistake (PSbMV) tolerance or resistance
to PSbMV for immunity. This mistake would not necessarily result from failure
to assay for the presence of PSbMV in inoculated plants, but from an under-
estimation of the extent to which gene Sbm can be modified, including simula-
tion of immunity.
If immunity, indeed, specifies that the pathogen cannot multiply in the
host at all or beyond the point of inoculation, then the term immunity is
purely qualitative and precludes systemic host infection. Therefore, the
difference between resistant and immune plants is the presence or absence,
respectively, of the systemic infection process. In the case of PSbMV, immune
pea plants would contain no detectable virus beyond the virus inoculated
tissues. Anything less than immunity becomes a quantitative phenomenon,
representing degrees of resistance with correspondingly lesser or greater
deleterious effect on plant performance.
30 RESEARCH REPORTS PNL Volume 12 1980
Indirect evidence from early efforts to breed for PSbMV-immunity, as
well as direct experimental evidence, suggest the existence of a "threshold
effect" in the identification of PSbMV-immune breeding progenies. That is,
progenies from certain PSbMV-immune parents may appear to be immune when
inoculated with PSbMV once or twice, but in fact become infected after three
or four inoculations. Such pseudo-immune plants, then, are able to transmit
PSbMV through their seeds and would therefore have the potential of trans-
mitting virus from inoculated progenies (screened for immunity) into succeeding
generations. It is hoped, on the basis of this evidence, that immunity would
be the only acceptable breeding objective, an objective warranting precise
virus-detection methodology.
1. Baggett, J. R. and R. 0. Hampton. 1972. Plant Dis. Rept. 56:131-132.
2. Hampton, R., G. Mink, L. Bos, M. Inouye and D. Hagedorn. 1980. Nether-
lands Journal of Plant Pathology (In press).
3. Hagedorn, D J. and E. T. Gritton. 1973. Phytopathology 63:1130-1133.
4. Hampton, R. 0. 1972. Phytopathology 62:268-272.