RESISTANCE TO RUSTS IN HARD PINES 451 



rust galls exist in proximity and otherwise similar conditions to those 

 with none (Peterson, 1960; York, 1929). That such striking differences 

 are genetically determined is probable, but has not yet been clearly 

 demonstrated. Results of inoculation of ponderosa pine progenies from 

 heavily infected and rust-free parents growing at the Institute of Forest 

 Genetics, Placerville, California, have been inconclusive (unpublished 

 data) . Although no parent tested was found to transmit a high degree of 

 resistance to its offspring, marked variation among individual trees was 

 found in the type and rate of symptom development. Several trees with- 

 stood repeated inoculation (Quick, 1966). These results were very similar 

 to those of Hutchinson (1935) and True (1938) , who made numerous field 

 inoculations of planted Scots pine in New York. 



NECHANISMS OF RESISTANCE 



Siggers (1955) proposed that differences in the phenological develop- 

 ment of trees might be causally associated with corresponding differences 

 in susceptibility to fusiform rust. He reasoned that trees that broke 

 winter dormancy earlier would be more in phase with the seasonal develop- 

 ment of the pathogen and would expose succulent, susceptible new shoots 

 to the basidiospore stage for a longer period of time. The greater 

 susceptibility of trees that had been cultivated and fertilized (Gilmore 

 and Livingston, 1958), planted on old fields (with presumably high 

 residual fertility) (Siggers and Lindgren, 1947), or exposed to fire was 

 attributed to an induced early break in dormancy. No definitive evidence 

 to support this hypothesis has been advanced, however, and it can be 

 argued equally plausibly that shoots that develop sooner also harden off 

 sooner and become more resistant. True (1938) found that resistance in 

 Scots pine to the so-called Woodgate rust (P. harknessii) increased with 

 age of shoots during a single season. He observed that aeciospore germ 

 tubes penetrated the cuticle and epidermis of resistant and susceptible 

 hosts alike, but only in less lignified portions of the shoot before 

 periderm formation. It seems likely that most pathogens that have shoots 

 (as opposed to needles) as their primary infection courts would meet with 

 the kind of functional, ontogenetic resistance described. The critical 

 questions are how strongly variation in seasonal phenology or rate of 

 maturation are inherited, and whether they are genetically correlated 

 with varying degreees of susceptibility. In jack pine, at least, the 

 evidence is negative--seed sources that differed in susceptibility to 

 eastern gall rust all broke dormancy at about the same time (McGrath, 

 1967). 



Experience with crop diseases, especially rusts, has taught that 

 resistance is more often a dynamic process of host response to a pathogen 

 on a protoplasmic level than a static precondition of the host. 

 Hutchinson (1935) and True (1938) identified three general types of host 

 response following field inoculation of phenotypically resistant and 

 susceptible trees of Scots pine with P. harknessii: (a) typical gall 

 formation of susceptible hosts; (b) atypical, often abortive gall forma- 

 tion of partially resistant hosts, characterized by cracked, resinous 

 bark; and (c) small necrotic spots, occasionally followed by slight 

 swellings that failed to develop further, on resistant hosts. Although 

 Scots pine is not a natural host of P. harknessii , similar symptoms 

 found on ponderosa and other native pines (York, 1938; Quick, 1966) 

 suggest that these responses were characteristic. 



