Genome scans on experimentally evolved populations reveal candidate regions for adaptation to plant resistance in the potato cyst nematode Globodera pallida.

Improving resistance durability involves to be able to predict the adaptation speed of pathogen populations. Identifying the genetic bases of pathogen adaptation to plant resistances is a useful step to better understand and anticipate this phenomenon. Globodera pallida is a major pest of potato crop for which a resistance QTL, GpaVvrn , has been identified in Solanum vernei. However, its durability is threatened as G. pallida populations are able to adapt to the resistance in few generations. The aim of this study was to investigate the genomic regions involved in the resistance breakdown by coupling experimental evolution and high-density genome scan. We performed a whole-genome resequencing of pools of individuals (Pool-Seq) belonging to G. pallida lineages derived from two independent populations having experimentally evolved on susceptible and resistant potato cultivars. About 1.6 million SNPs were used to perform the genome scan using a recent model testing for adaptive differentiation and association to population-specific covariables. We identified 275 outliers and 31 of them, which also showed a significant reduction in diversity in adapted lineages, were investigated for their genic environment. Some candidate genomic regions contained genes putatively encoding effectors and were enriched in SPRYSECs, known in cyst nematodes to be involved in pathogenicity and in (a)virulence. Validated candidate SNPs will provide a useful molecular tool to follow frequencies of virulence alleles in natural G. pallida populations and define efficient strategies of use of potato resistances maximizing their durability.

Origin and genetic diversity of Western European populations of the potato cyst nematode (Globodera pallida) inferred from mitochondrial sequences and microsatellite loci.

Native to South America, the potato cyst nematode Globodera pallida is one of the principal pests of Andean potato crops and is also an important global pest following its introduction to Europe, Africa, North America, Asia and Oceania. Building on earlier work showing a clear south to north phylogeographic pattern in Peruvian populations, we have been able to identify the origin of Western European populations with high accuracy. They are all derived from a single restricted area in the extreme south of Peru, located between the north shore of the Lake Titicaca and Cusco. Only four cytochrome b haplotypes are found in Western Europe, one of them being also found in some populations of this area of southern Peru. The allelic richness at seven microsatellite loci observed in the Western European populations, although only one-third of that observed in this part of southern Peru, is comparable to the allelic richness observed in the northern region of Peru. This result could be explained by the fact that most of the genetic variability observed at the scale of a field or even of a region is already observed at the scale of a single plant within a field. Thus, even introduction via a single infected potato plant could result in the relatively high genetic variability observed in Western Europe. This finding has important consequences for the control of this pest and the development of quarantine measures.

Molecular approaches to the taxonomic position of Peruvian potato cyst nematodes and gene pool similarities in indigenous and imported populations of Globodera.

Peruvian potato cyst nematode populations were analysed to assess both their inter- and intraspecific similarities. ITS--RFLP and two satellite DNA sequences were used as taxonomic tools. Both techniques have confirmed that the Peruvian populations have as their closest relatives the European Globodera pallida, despite the detection of clear differences that prevents us from assigning these South American populations unambiguously to any Globodera species. A more precise study of the variability of these Peruvian populations was investigated and they were compared with the imported European populations using protein (2-DGE) and DNA (RAPD) datasets. The clear distinction between the Peruvian and the European populations was confirmed and, inside each group, no correlation was found between the pathotype classification and the observed clustering of the populations. Surprisingly, while RAPDs revealed a higher variability in the Peruvian group than in the European one, some characteristic proteins were found by 2-DGE in some European populations, whereas it was impossible to find any in the Peruvian populations. It is concluded that the primary founders of the European populations may have an origin other than that of the Peruvian populations involved in this study.

Human recombinant growth hormone increases small bowel lengthening after massive small bowel resection in piglets.

BACKGROUND/PURPOSE: Dramatic improvement in small bowel lengthening and in weight gain has been demonstrated in newborn rats treated with human growth hormone (GH) after massive small bowel resection. The aim of this study was to confirm these results in another animal model and to specify the part food intake plays in small bowel lengthening induced by GH. METHODS: Twenty-five piglets underwent laparotomy at day 28 of life. Intestinal length was measured under general anesthesia, and animals had an 80% resection of small bowel, leaving a similar length of jejunum and ileon. There were no perioperative deaths. One animal died 3 days after surgery. Animals were assigned to five groups: (1) S (n = 4): sham, mere laparotomy; (2) GH-S (n = 4): sham and GH treatment (0.1 IU/kg/d subcutaneously); (3) R (n = 7): intestinal resection; (4) GH-R (n = 6); and (5) GH-R AdL (n = 4): intestinal resection and GH treatment. S, GH-R, and GH-R AdL had a free diet; GH-S and GH-R were pair-fed with S and R, respectively. Animals were killed 28 days later. RESULTS: Weight gain was not different in the two nonresected groups (S, 144 +/- 6% of initial weight; GH-S, 150 +/- 3%) and was significantly higher than in the resected groups (R, 67 +/- 28%; GH-R, 74 +/- 16%; GH-R AdL, 55 +/- 16%; NS). GH did not enhance small bowel lengthening in the nonresected groups; S, 41.9 +/- 23% and GH-S, 36.9 +/- 9%, in sharp contrast with the resected groups; R, 28 +/- 9 cm versus GH-R, 96 +/- 39 cm (P = .0008) and versus GH-R AdL, 89 +/- 41 cm (P = .003). Compared with initial length, the increase was R, 16.2 +/- 5%; GH-R, 56.5 +/- 24%; GH-R AdL, 51 +/- 25%. Villus height and diameter, average number of mitosis per field, intestinal muscular layer, wall thickness, and crypt ratio were higher in resected groups than in unresected ones, with no difference observed between resected groups. CONCLUSIONS: GH improves the postoperative intestinal adaptation process after massive small bowel resection in newborn piglets in terms of small bowel lengthening. In contrast to rats, GH did not improve weight gain. In addition, no difference was observed whether animals were on a free or a controlled diet.