PEA SEEDBORNE MOSAIC SYMPTOM VARIATION AMONG PISUM PLANT INTRODUCTION ACCESSIONS: EXPRESSIONS AND VARIATION IN SYMPTOM EXPRESSION AMONG DIFFERENT GENOTYPES OF PISUM AND THE PATHOLOGICAL IMPLICATIONS

PNL Volume 12 1980 RESEARCH REPORTS 29

PEA SEEDBORNE MOSAIC SYMPTOM VARIATION AMONG PISUM PLANT INTRODUCTION

ACCESSIONS: EXPRESSIONS AND VARIATION IN SYMPTOM EXPRESSION AMONG DIFFERENT

GENOTYPES OF PISUM AND THE PATHOLOGICAL IMPLICATIONS

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.