Marie-Claire Kerlan

Risk assessment of outcrossing of transgenic rapessed to related species

SummaryThe risk for a gene dispersal is reported for reciprocal crosses between a transgenic rapeseed variety resistant to the herbicide phosphinotricin and five related species. The first stages after pollination were cytologically observed and fertilized ovaries were established in in vitro culture for the production of interspecific hybrids. A similar classification was observed for the index of pollination compatibility and embryo yield. From the 243 embryos produced, 109 plantlets were obtained in a greenhouse. All the interspecific combinations tested were able to produce hybrid plants. A higher number of hybrids was obtained when rapeseed was used as the female parent. The hybrids had the expected triploid structure except for two amphidiploid, B. napus × B. oleracea, and one amphidiploid, B. napus × S. arvensis, plants with 56 chromosomes. The triploid hybrids were sterile or partially fertile but two of the amphidiploid plants, B. napus × B. oleracea, were fully fertile. The cytoplasm source did not seem to affect the fertility of the hybrids.

Resistance Quantitative Trait Loci Originating from Solanum sparsipilum Act Independently on the Sex Ratio of Globodera pallida and Together for Developing a Necrotic Reaction

Plant resistance to nematodes is related to the ability of the host to reduce the development of nematode juveniles into females. Resistance to the potato cyst nematode (PCN) Globodera pallida, originating from the wild species Solanum sparsipilum, was dissected by a quantitative trait loci (QTL) approach. Two QTL explained 89% of the phenotypic variation. The QTL GpaV(s)spl on chromosome V displayed the major effect on the cyst number (coefficient of determination [R2] = 76.6%). It restricted G. pallida development to 16.2% of juveniles, 81.5% of males, and 2.3% of females. The QTL GpaXI(s)spl on chromosome XI displayed a lower effect on the cyst number (R2 = 12.7%). It restricted G. pallida development to 13.8% of juveniles, 35.4% of males, and 50.8% of females. Clones carrying both QTL restricted the nematode development to 58.1% juveniles, 41.1% of males, and 0.8% of females. We demonstrated that potato clones carrying both QTL showed a strong necrotic reaction in roots infected by nematodes, while no such reaction was observed in clones carrying a single QTL. This result underlines the importance to introgress together GpaV(s)spl and GpaXI(s)spl into potato cultivars, in order to reduce the density of this quarantine pest in soil and to decrease the risk of selecting overcoming G. pallida subpopulations.

Resistance to the root-knot nematode Meloidogyne fallax in Solanum sparsipilum: analysis of the mechanisms.

The genotype 88S.329.15 of Solanum sparsipilum was studied in order to analyse the genetic basis and the mechanisms of its resistance to Meloidogyne fallax . In infected plants grown at 20°C, juveniles invaded the root system with a clear delay and a lower infection rate in comparison to the susceptible S. tuberosum genotype BF15 H1. No defence reaction occurred during root invasion and migration toward the vascular cylinder. The juveniles induced development of feeding sites usually composed of several giant cells, which contained condensed cytoplasm, only small vacuoles, enlarged nuclei with pronounced nucleoli and almost no endoplasmic reticulum. Abundant necrosis of surrounding parenchymatous vascular cylinder cells lead to the degeneration of the giant cells. More than 90% of the invading juveniles failed to develop. The others developed as males. The resistance inheritance was analysed on 128 F1 hybrids obtained using the susceptible line BF15 H1 as the female parent and 88S.329.15 as the male parent. Among the progenies, 68 genotypes produced a necrotic reaction to nematode infection and 60 produced no necrosis. This 1 : 1 segregation pattern suggests a monogenic control of this defence reaction. Unlike the resistant parent 88S.329.15, some M. fallax females developed in the roots of necrotically responding hybrids. There was a normal distribution of mean numbers of adult females found in the roots of these genotypes. This result suggests that the ability of the resistant genotype 88S.329.15 to suppress development of females is quantitatively inherited and likely to be controlled by more than one locus. These data indicate that the mechanism of resistance is different from the resistance to Meloidogyne incognita conferred by the Mi gene of tomato.

Quantitative Resistance to Plant Pathogens in Pyramiding Strategies for Durable Crop Protection

Quantitative resistance has gained interest in plant breeding for pathogen control in low-input cropping systems. Although quantitative resistance frequently has only a partial effect and is difficult to select, it is considered more durable than major resistance (R) genes. With the exponential development of molecular markers over the past 20 years, resistance QTL have been more accurately detected and better integrated into breeding strategies for resistant varieties with increased potential for durability. This review summarizes current knowledge on the genetic inheritance, molecular basis, and durability of quantitative resistance. Based on this knowledge, we discuss how strategies that combine major R genes and QTL in crops can maintain the effectiveness of plant resistance to pathogens. Combining resistance QTL with complementary modes of action appears to be an interesting strategy for breeding effective and potentially durable resistance. Combining quantitative resistance with major R genes has proven to be a valuable approach for extending the effectiveness of major genes. In the plant genomics era, improved tools and methods are becoming available to better integrate quantitative resistance into breeding strategies. Nevertheless, optimal combinations of resistance loci will still have to be identified to preserve resistance effectiveness over time for durable crop protection.

Phenotypic and Genomic Modifications Associated with Globodera pallida Adaptation to Potato Resistances

Studying phenotypic and genomic modifications associated with pathogen adaptation to resistance is a crucial step to better understand and anticipate resistance breakdown. This short review summarizes recent results obtained using experimentally evolved populations of the potato cyst nematode Globodera pallida. In a first step, the variability of resistance durability was explored in four different potato genotypes carrying the resistance quantitative trait loci (QTL) GpaVvrn originating from Solanum vernei but differing by their genetic background. The consequences of the adaptation to resistance in terms of local adaptation, cross-virulence and virulence cost were then investigated. Finally, a genome scan approach was performed in order to identify the genomic regions involved in this adaptation. Results showed that nematode populations were able to adapt to the QTL GpaVvrn, and that the plant genetic background has a strong impact on resistance durability. A trade-off between the adaptations to different resistant potato genotypes was detected, and we also showed that adaptation to the resistance QTL GpaVvrn from S. vernei did not allow adaptation to the colinear locus from S. sparsipilum (GpaVspl). Unexpectedly, the adaptation to resistance led to an increase of virulent individual’s fitness on a susceptible host. Moreover, the genome scan approach allowed the highlighting of candidate genomic regions involved in adaptation to host plant resistance. This review shows that experimental evolution is an interesting tool to anticipate the adaptation of pathogen populations and could be very useful for identifying durable strategies for resistance deployment.