Euphytica 112: 211–217, 2000. © 2000 Kluwer Academic Publishers. Printed in the Netherlands. 211 Qualitative resistance of Hevea to Phyllachora huberi P. Henn Vincent Le Guen 1 , Marc Seguin 2 & Carlos R.R. Mattos 3 1 Cirad, BP 701, Kourou Cedex, 97387 French Guyana; 2 Cirad, Avenue Agropolis (Bat 3), BP 5035 – 34032 Montpellier Cedex 1, France; 3 Michelin, Plantações Michelin da Bahia Ltda, Caixa Postal 02, Ituber´ a 45435-000 (BA), Brazil Received 19 October 1998; accepted 16 September 1999 Key words: Hevea sp., isozyme markers, monogenic resistance, Phyllachora huberi, physiological race, qualitative resistance Summary Qualitative observations of Hevea spp. resistance to Phyllachora huberi were carried out on 200 clones in a collection and 21 full-sib progenies under natural conditions of infestation. A total of 42 clones, mostly originating from the natural range of the Hevea genus, and at least two species (H. brasiliensis and H. benthamiana) revealed total resistance to the parasite. For nine of the thirteen ‘resistant × susceptible’ and ‘resistant × resistant’ progenies studied, the ratio of susceptible: resistant plants suggested the existence of a total resistance mechanism produced by a dominant allele at a single locus for the P. huberi race(s) present at the study site. For three of the progenies involving the same resistant parent, it was possible to locate the gene (called Phr) at 14.7 cm from the adh isozyme locus. Abbreviations: A – Amazonian survey clones; B – Hevea benthamiana;P– Hevea pauciflora; W – Wickham, clones originated from genotypes introduced into Asia in 1876 Introduction Although it was first described almost a century ago, the Hevea leaf parasite Phyllachora huberi P. Henn., which causes black crust disease, has never promp- ted any in-depth studies. The range of the disease is restricted to the Amazonian region. Infection by P. huberi results in the appearance of small shiny black crusts 5 to 10 mm in diameter visible on the lower surface of the leaves (Vincens, 1915). The crusts are formed by perithecia or conidiophores that can release 14–18 × 8–10 μm ascospores (Roger, 1953) or 10– 15 × 3–5 μm conidia (Vincens, 1915), respectively. Langford et al. (1954) reported that the fungus de- velops very slowly on the leaves and that no visible lesion develops on leaves less than a month old. Also according to Vincens (1915), the leaves seem barely to suffer from the presence of the parasite and the disease is usually limited to foci that are relatively easy to treat. Roger (1953) reported that the ‘spe- cies is quite common ... and it mainly attacks adult leaves. In the severest cases, leaflets dry out, turn red and fall, but only a short time before the nor- mal date for them to fall’. Langford (1953) noted that the main damage caused to Hevea by P. huberi is to favour infection by secondary fungi such as Glomer- ella cingulata, and that the only step to be taken is to avoid planting extremely susceptible clones. More re- cently, Junqueira & Bezerra (1990) identified another fungus, Rosenscheldiella heveae, whose lesion is al- most systematically associated with that of P. huberi, and proposed in that case to call the disease ‘black crust complex’. In Hevea, there are very marked differences in clonal susceptibility to P. huberi, in both qualitative terms (existence or absence of black crusts) and quant- itative terms (number of lesions per unit leaf area and mean lesion diameter). This study primarily looks at qualitative resistance.