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Summary We have established culture conditions for successful infection and development of several economically important cyst‐forming and root‐knot nematodes on Arabidopsis thaliana under monoxenic conditions. Complete life cycles were obtained with the sedentary cyst nematodes Heterodera schachtii, H. trifolii, H. cajani and the root‐knot nematodes Meloidogyne incognita and M. arenariaas well as with the migratory nematode Pratylenchus penetrans. In contrast, H. goettingiana and Globodera rostochiensis were unable to develop on Arabidopsis roots. Tissue‐culture quality agar and medium conditions optimized for hydroponic root culture were essential for successful infections. Detailed in‐vivo observations were made inside Arabidopsis roots during the early infection stages of M. incognita and during complete development of H. schachtii. Seventy‐four different ecotypes of Arabidopsis were screened for their susceptibility towards H. schachtii resulting in a range of infection rates. None of the ecotypes tested showed complete resistance in vitro. The use of Arabidopsis as a host for plant‐parasitic nematodes will provide a new model system for the molecular genetic analysis of this interaction.

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SUMMARYMost aphid species (Hemiptera : Aphididae) are parthenogenetic between periods of sexual reproduction. They are also highly polyphenic, with different adult morphs occurring in the life cycle, i . winged, wingless, asexual and sexual. It is assumed that aphids born in a parthenogenetic clonal lineage are genetically identical regardless of the final adult form (with the exception of sexual forms). Using the randomly amplified polymorphic DNA-polymerase chain reaction (RAPD-PCR) we have found that different asexual adult phenotypes (winged and wingless) of some clones of two cereal aphid species (the grain aphid, Sitobion a enae (F.) and the bird-cherry aphid, Rhopalosiphum padi (L.)) may be distinguished by the presence or absence of one or more RAPD-PCR bands. In three of nine clones examined, such differences were found, and Southern blotting and hybridization of the discriminating bands confirmed these to be of aphid origin, rather than due to endosymbiotic bacteria or contaminating fungi. The main 248 and 296 bp bands, in the two species, respectively, were sequenced and found to be A\T rich. The smaller band showed 57 % homology with white striated muscle over a stretch of 90 bp. Genomic DNA treated with dimethyl sulphoxide to remove secondary structures still showed differences in RAPD-PCR profiles between winged and wingless morphs within the unusual clones. This discovery may be widespread and therefore it is important to understand the phenomenon in relation to clonal organisms.

Type IV collagen forms a network that provides the major structural support of basement membranes. We have determined the nucleotide alterations and phenotypes of 17 mutant alleles of the Caenorhabditis elegans alpha 2(IV) collagen gene let‐2. All 17 mutations are within the triple helical (Gly‐X‐Y) repeat domain of the molecule. Fifteen of the mutations are replacements of Gly‐X‐Y repeat glycines with aspartate, glutamate or arginine, and they cause a wide range of phenotypes. The mildest alleles are nearly wild‐type at 15 and 20 degrees C but embryonic lethal at 25 degrees C, while the most severe allele is embryonic lethal at all three temperatures. Mutations resulting in severe phenotypes are generally located in areas of lower calculated thermal stability of the type IV collagen molecule. An alanine to threonine substitution at position X of a Gly‐X‐Y triplet immediately following an interruption results in a severe phenotype. This mutation is unusual because substitutions at positions X or Y have not generally been found to cause strong phenotypes in C. elegans or human collagens. An intron splice acceptor mutation causes a strict embryonic lethal phenotype, but does not completely abolish gene function. Pairs of independent mutations affect each of three glycines, indicating a non‐random distribution of mutations in the molecule. It is suggested that this clustering results because many glycine substitutions may cause dominant lethal or sterile phenotypes.