A large cohort study of 74,828 benzene‐exposed and 35,805 unexposed workers employed between 1972 and 1987 in 12 cities in China were followed to determine mortality from all causes and the incidence of lymphohematopoietic malignancies and other hematologic disorders. Benzene‐exposed study subjects were employed in a variety of occupations, including painting, printing, and the manufacture of footwear, paint, and other chemicals. All‐cause mortality was similar in the benzene‐exposed and unexposed comparison group. Statistically significant excess deaths were noted among benzene‐exposed subjects for leukemia (RR = 2.3, 95% Cl: 1.1–5.0), malignant lymphoma (RR = 4.5, 95% Cl: 1.3–28.4), and non‐neoplastic diseases of the blood (RR = ∞, 95% Cl: 2.5‐∞), and a marginally significant excess was noted for lung cancer (RR = 1.4, 95% Cl: 1.0–2.0). Risk was significantly elevated for the incidence of all lymphohematopoietic malignancies (RR = 2.6, 95% Cl: 1.5–5.0), malignant lymphoma (RR = 3.5, 95% Cl: 1.2–14.9), and leukemia (RR = 2.6, 95% Cl: 1.3–5.7). Among the leukemia subtypes, only acute myelogenous leukemia (AML) incidence was significantly elevated (RR = 3.1, 95% Cl: 1.2–10.7), although nonsignificant excesses were also noted for chronic myelogenous leukemia (CML) (RR = 2.6, 95% Cl: 0.7–16.9) and lymphocytic leukemias (RR = 2.8, 95% Cl: 0.5–54.5). Significant excesses were found for aplastic anemia (RR = ∞, 95% Cl: 2.2‐∞) and myelodysplastic syndrome (RR = ∞, 95% Cl: 1.7‐∞). Employment in benzene‐associated occupations in China is associated with a wide spectrum of myelogenous and lymphocytic malignant diseases and related disorders. Investigations continue to assess the nature of these associations. © 1996 Wiley‐Liss, Inc.

Resistance in tomato against race 1 strains of the fungal vascular wilt pathogens Verticillium dahliae and V. albo-atrum is mediated by the Ve locus. This locus comprises two closely linked inversely oriented genes, Ve1 and Ve2, which encode cell surface receptors of the extracellular leucine-rich repeat receptor-like protein (eLRR-RLP) type. While Ve1 mediates Verticillium resistance through monitoring the presence of the recently identified V. dahliae Ave1 effector, no functionality for Ve2 has been demonstrated in tomato. Ve1 and Ve2 contain 37 eLRRs and share 84% amino acid identity, facilitating investigation of Ve protein functionality through domain swapping. In this study it is shown that Ve chimeras in which the first thirty eLRRs of Ve1 were replaced by those of Ve2 remain able to induce HR and activate Verticillium resistance, and that deletion of these thirty eLRRs from Ve1 resulted in loss of functionality. Also the region between eLRR30 and eLRR35 is required for Ve1-mediated resistance, and cannot be replaced by the region between eLRR30 and eLRR35 of Ve2. We furthermore show that the cytoplasmic tail of Ve1 is required for functionality, as truncation of this tail results in loss of functionality. Moreover, the C-terminus of Ve2 fails to activate immune signaling as chimeras containing the C-terminus of Ve2 do not provide Verticillium resistance. Furthermore, Ve1 was found to interact through its C-terminus with the eLRR-containing receptor-like kinase (eLRR-RLK) interactor SOBIR1 that was recently identified as an interactor of eLRR-RLP (immune) receptors. Intriguingly, also Ve2 was found to interact with SOBIR1.

Plant-pathogenic microbes secrete effector molecules to establish themselves on their hosts, whereas plants use immune receptors to try and intercept such effectors in order to prevent pathogen colonization. The tomato cell surface-localized receptor Ve1 confers race-specific resistance against race 1 strains of the soil-borne vascular wilt fungus Verticillium dahliae which secrete the Ave1 effector. Here, we describe the cloning and characterization of Ve1 homologues from tobacco (Nicotiana glutinosa), potato (Solanum tuberosum), wild eggplant (Solanum torvum) and hop (Humulus lupulus), and demonstrate that particular Ve1 homologues govern resistance against V. dahliae race 1 strains through the recognition of the Ave1 effector. Phylogenetic analysis shows that Ve1 homologues are widely distributed in land plants. Thus, our study suggests an ancient origin of the Ve1 immune receptor in the plant kingdom.

SUMMARYVerticillium wilt, caused by soil-borne fungi of the genus Verticillium, is an economically important disease that affects a wide range of host plants. Unfortunately, host resistance against Verticillium wilts is not available for many plant species, and the disease is notoriously difficult to combat. Host-induced gene silencing (HIGS) is an RNA interference (RNAi)-based process in which small RNAs are produced by the host plant to target parasite transcripts. HIGS has emerged as a promising strategy for the improvement of plant resistance against pathogens by silencing genes that are essential for these pathogens. Here, we assessed whether HIGS can be utilized to suppress Verticillium wilt disease by silencing three previously identified virulence genes of V. dahliae (encoding Ave1, Sge1 and NLP1) through the host plants tomato and Arabidopsis. In transient assays, tomato plants were agroinfiltrated with Tobacco rattle virus (TRV) constructs to target V. dahliae transcripts. Subsequent V. dahliae inoculation revealed the suppression of Verticillium wilt disease on treatment with only one of the three TRV constructs. Next, expression of RNAi constructs targeting transcripts of the same three V. dahliae virulence genes was pursued in stable transgenic Arabidopsis thaliana plants. In this host, V. dahliae inoculation revealed reduced Verticillium wilt disease in two of the three targets. Thus, our study suggests that, depending on the target gene chosen, HIGS against V. dahliae is operational in tomato and A. thaliana plants and may be exploited to engineer resistance in Verticillium wilt-susceptible crops.

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