Genetic Differences In Resistance Research Articles

New Insights into the Fungal Diversity of Cranberry Fruit Rot in Québec Farms Through a Large-Scale Molecular Analysis.

Cranberry fruit rot (CFR) pathogens are widely reported in the literature, but performing large-scale analysis of their presence inside fruit has always been challenging. In this study, a new molecular diagnostic tool, capable of identifying simultaneously 12 potential fungal species causing CFR, was used to better define the impact of CFR across cranberry fields in Québec. For this purpose, 126 fields and 7,825 fruits were sampled in three cranberry farms distributed throughout the province and subjected to comparative analyses of fungal presence and abundance according to cultural practices, sampling times, and cranberry cultivars. All 12 pathogens were detected throughout the study, but as a first major finding, the analyses revealed that four species, Godronia cassandrae, Colletotrichum fructivorum, Allantophomopsis cytisporea, and Coleophoma empetri, were consistently predominant regardless of the parameters studied. Comparison of conventional and organic productions showed a significant reduction in fungal richness and relative abundance. Interestingly, Monilinia oxycocci was found almost exclusively in organic productions, indicating that fungicides had a strong and persistent effect on its population. Surprisingly, there were no significant differences in fungal relative abundance or species richness between fruit sampled at harvest or in storage, suggesting that there may not exist a clear distinction between field and storage rot, as was previously thought. Comparative analysis of fungal species found on eight different cranberry cultivars indicated that they were all infected by the same fungi but could not rule out differences in genetic resistance. This large-scale analysis allows us to draw an exhaustive picture of CFR in Québec and provides new information with respect to its management.

137 Randel Lecture: Genetic control of thermotolerance in cattle at the whole-animal and cellular level

Abstract Research by Randel and others has revealed the extensive genetic diversity in thermotolerance existing in cattle. Genetic differences in resistance to heat stress involve genes that affect body temperature regulation and that stabilize cellular function during hyperthermia. There are large differences between breeds in ability to regulate body temperature during heat stress. There is also genetic variation in thermoregulatory ability within breeds that arose in cold climates – the estimate of heritability of rectal temperature during heat stress in Holsteins is 0.17. Efforts are underway to identify genes conferring increased thermoregulatory ability in thermotolerant breeds and transfer these to thermosensitive breeds. One such gene is the prolactin receptor gene (PRLR). Several mutations in PRLR exist in criollo-type B. taurus that result in formation of a truncated receptor protein. Cattle with this mutation, which is dominant, have a short sleek hair coat and are referred to as “slick”. The slick mutation has been introduced into Holsteins by crossbreeding with Senepol cattle and in Red Angus by gene editing. Slick Holsteins are less affected by heat stress than wild-type Holsteins with respect to rectal temperature, milk yield and reproduction. Genetic variation also exists in cellular responses to elevated temperature (i.e., heat shock). Exposure of preimplantation embryos to heat shock, for example, causes a greater reduction in subsequent development of Angus, Holstein, Angus x Holstein or Jersey embryos than embryos from Brahman or Nelore (B. indicus) or Romosinuano (criollo). One gene with alleles affecting cellular resistance is the heat shock protein 70 gene HSPA1A. A mutation in the promoter region of HSPA1Ais associated with increased transcription of the encoded protein and enhanced survival of lymphocytes exposed to heat shock. Identification of other genes conferring thermotolerance will result in the increased ability to produce thermotolerant lines of cattle via genetic selection or gene transfer.

Fighting the Deadly Helminthiasis without Drug Resistance

Helminthiasis is a very costly management problem in the sheep and goat industry, because the gastrointestinal parasites develop resistance against all chemical products that are discovered and produced by the pharmaceutical industry. The use of natural herbal contents of tannin as especially in Sericea Lespedeza (SL; Lespedeza cuneate) is very promising. Utilizing genetic differences in resistance among the different goat and sheep breeds is a promising alternative, with limited success to date. Totally eliminating the offending parasites from re-infesting by plowing under affected pastures for some seasons, or scheduling rotational pastures, or feeding fresh (grazed) or dried forms of the perennial warm-season legume sericea lespedeza to the infected sheep and goats, or using elevated housing with slatted floors are the most promising alternatives to the ancient tradition of herding and managing ruminants by transhumance. An elevated slatted floor housing is desirable, and deserves wider attention because of its potential in controlling helminthiasis. Slatted floors are already used in the sheep and goat industries in Sweden, Norway, Malaysia and Guatemala.

Genome-wide association analysis for late blight resistance of potato resources

<p indent=0mm>The mining of broad-spectrum resistance genes is the basis of the breeding of potato varieties with high late blight resistance. In this study, 288 samples of late disease resistance selected by the International Potato Center (CIP) for years were planted and were investigated for two consecutive years, which could provide some theoretical and material basis for breeding of late blight resistant varieties and help to study on disease resistance mechanism. The late blight resistance of each sample was evaluated using AUDPC and sAUDPC values. The population simplified genome sequencing was performed by SLAF-seq and carried out by genome-wide association analysis in order to discover the genetic loci and candidate genes related to late blight resistance. There were wide genetic differences in resistance to late blight among 288 samples. Through genome-wide association analysis, based on five analytical models, a total of 82 loci significantly correlated with late blight resistance were identified. Combined with genomic annotation, there were 54 candidate genes known or likely to be associated with late blight resistance in the association interval. Among them, 23 genes were resistant genes, including late blight resistance gene <italic>R1</italic> homolog, <italic>Sw-5</italic> homolog (<italic>R8</italic>) and <italic>Rpi-vnt1</italic>, as well as gene encoding pleiotropic resistance protein. Five genes encoded MAPK protein and WRKY transcription factor; one gene was involved in the JA pathway; three genes were associated with salicylic acid pathway; six genes were related to the course of the disease; three genes were involved in the synthesis of phenylpropionic acid. Other genes related to resistance to late blight included HMGR gene (2) and cytochrome P450 (21).

Genomic evaluation of resistance to Haemonchus contortus in a South African Dohne Merino flock

The aim of this study was to use genome-wide SNP data to investigate phenotypic and genetic differences in resistance to Haemonchus contortus between resistant and susceptible South African Dohne Merino sheep. The participating farm (Wauldby) has a history of heavy H. contortus challenge and implemented a selection strategy for resistance to H. contortus in 2011. Faecal egg count (FEC), body condition scores (BCS) and Famacha© scores (FAM) were recorded annually on lambs from weaning in January until the end of June from 2011 to 2014. Animals with FAM scores of ≥ 2.5 or BCS scores < 1.5 were subjected to anthelmintic treatment and recorded as “Dosed” animals. Animals (196) were selected for genotyping based on EBV for FEC and classified into Case and Control groups on the basis of whether they were dosed or not. The Grootfontein Dohne Merino flock has never been subjected to selection for resistance to gastrointestinal parasites and 48 animals were selected on FEC for genotyping. DNA obtained from blood samples were genotyped using the Illumina® Ovine SNP50 BeadChip. Principal component analysis (PCA) resulted in four distinct genetic clusters, with the Grootfontein sheep population clustering separately. The Wauldby animals in Cluster 3 had significantly lower FEC and higher BCS than the animals in Clusters 2 and 4. FEC breeding values of 114 ± 97, -629 ± 84 and -2 ± 45 were recorded for PCA-based Genetic cluster 2, 3 and 4 animals, respectively. The majority (88%) of animals in Cluster 3 were the progeny of sires from the resistant line. The average number of runs of homozygosity (ROH) was 44, 46, 54 and 47 per animal for Clusters 1, 2, 3 and 4 respectively. The highest number of ROHs was found on chromosomes 1, 2, 3, 4, 6, 9 and 10, on which QTL for resistance traits have been identified previously. Sires in Genetic cluster 3 were highly resistant and can be used in a breeding program to develop H. contortus resistant sheep. The results indicated genetic variation in host resistance against H. contortus in the Wauldby flock and breeding for resistance against nematodes is feasible.

Genetic Differences in Resistance of Scotch Pine to Eastern Pineshoot Borer

Genetic Differences in Resistance of Scotch Pine to Eastern Pineshoot Borer

Analysis of Differentially Expressed Genes in Necrotic Enteritis-infected Fayoumi Chickens using RNA Sequencing.

We identified and evaluated differentially expressed genes (DEGs) by RNA-Sequencing (RNA-Seq) in the intestinal mucosa of two Fayoumi chicken lines, M5.1 and M15.2, that are affected by necrotic enteritis (NE); these chicken lines share the same genetic background but have different major histocompatibility complexes. RNA-Seq generated over 49 and 40 million reads for lines M5.1 and M15.2, respectively. The alignment of these sequences with the Gallus gallus genome database revealed the expression of more than 14,500 genes in two lines, among which 581, 1270, and 1140 DEGs were detected when lines M15.2 and M5.1 were compared with the control and compared between each other. The analysis of all DEGs using the gene ontology database revealed annotations for 111 biological processes, 32 cellular components, and 17 molecular functions, and KEEG pathway mapping indicated that the DEGs were primarily involved in immunity, responses to various stimuli, and signal transduction. In addition, we analyzed 183 innate immune genes that were differentially expressed in NE-induced chicken lines, including 46 CD molecular genes, 89 immune-related genes, and 13 β-defensin genes with 3 lineage-specific duplications. Taken together, the transcriptional profiles showed that line M5.1 was more resistant to NE than line M15.2 and that differential gene expression patterns were associated with host genetic differences in resistance to NE. qRT-PCR and RNA-Seq analyses showed that all the genes examined had similar responses to NE (correlation coefficient R=0.84 to 0.88, p<0.01) in both lines. To the best of our knowledge, this is the first study that describes NE-induced DEGs using RNA-seq in two lines with different levels of susceptibility to NE. These results will lead to increased insights on NE disease resistance mechanisms and the role of host genes in the control of the host immune response.

On the Genetic Interpretation of Disease Data

BackgroundThe understanding of host genetic variation in disease resistance increasingly requires the use of field data to obtain sufficient numbers of phenotypes. We introduce concepts necessary for a genetic interpretation of field disease data, for diseases caused by microparasites such as bacteria or viruses. Our focus is on variance component estimation and we introduce epidemiological concepts to quantitative genetics.Methodology/Principal FindingsWe have derived simple deterministic formulae to predict the impacts of incomplete exposure to infection, or imperfect diagnostic test sensitivity and specificity on heritabilities for disease resistance. We show that these factors all reduce the estimable heritabilities. The impacts of incomplete exposure depend on disease prevalence but are relatively linear with the exposure probability. For prevalences less than 0.5, imperfect diagnostic test sensitivity results in a small underestimation of heritability, whereas imperfect specificity leads to a much greater underestimation, with the impact increasing as prevalence declines. These impacts are reversed for prevalences greater than 0.5. Incomplete data recording in which infected or diseased individuals are not observed, e.g. data recording for too short a period, has impacts analogous to imperfect sensitivity.Conclusions/SignificanceThese results help to explain the often low disease resistance heritabilities observed under field conditions. They also demonstrate that incomplete exposure to infection, or suboptimal diagnoses, are not fatal flaws for demonstrating host genetic differences in resistance, they merely reduce the power of datasets. Lastly, they provide a tool for inferring the true extent of genetic variation in disease resistance given knowledge of the disease biology.

Physical Function Is Weakly Associated with Angiotensin-Converting Enzyme Gene I/D Polymorphism in Elderly Japanese Subjects

Background: The turning point in the deterioration of physical function seems to occur between the ages of 70 and 80 years. In particular, muscle strength may decline even more in subjects older than 75. A recent study found that the angiotensin-converting enzyme (ACE) genotype also affects physiological left ventricular hypertrophy. A very limited number of papers have examined genetic differences in resistance and endurance forms of a single sporting discipline. Objective: The purpose of this study was to evaluate the relationship between ACE genotype and physical function by controlling the known confounding factors including dental status. Methods:We selected 431 subjects who were aged 76 years and did not require special care for their daily activities. We conducted a medical examination, followed by 5 physical function tests, as follows: (1) maximum hand grip strength, (2) maximal isometric knee extensor strength, (3) maximal stepping rate for 10 s, (4) one-leg standing time with eyes open and (5) 10-meter maximum walking speed. Subjects were genotyped for the ACE intron 16 Alu insertion. In addition, serum concentrations of total cholesterol, total protein, IgA and IgG were measured at a commercial laboratory. The Eichner index was used as an indicator of occlusal condition. Multiple linear regression analysis was performed to evaluate the relationship between the ACE gene insertion/deletion (I/D) polymorphism and physical function considering confounding factors. Results: The ACE gene I/D polymorphism was positively associated with hand grip strength and 10-meter maximum walking speed. Betas of hand grip strength were 0.09 for I/D (p = 0.022) and 0.12 for insertion/insertion (I/I; p = 0.004). Betas of 10-meter walking speed were –0.11 for I/D (p = 0.093) and –0.14 for I/I (p = 0.039). Dental status such as Eichner index class C was significantly associated with one-leg standing time with eyes open (beta –0.11; p = 0.028). Conclusion: This study suggests that there is a significant relationship between ACE genotype and physical function. In particular, subjects with the ACE deletion/deletion genotype were associated with upper extremities.

Susceptibility of four inbred mouse strains to a low-pathogenic isolate of Yersinia enterocolitica

EUMORPHIA (European Union Mouse Research for Public Health and Industrial Application) is a research program involved in developing new approaches in phenotyping, mutagenesis, and informatics to improve characterization of mouse models for understanding human physiology and disease. Secondary screen experiments include the development of assays to identify mice with altered susceptibility or resistance to infections. In this context we developed a new model and established a standard operating procedure for the experimental infection of mice with Yersinia (Y.) enterocolitica. In contrast with previous studies that dealt with high-pathogenic Y. enterocolitica, we used the low-pathogenic Y. enterocolitica strain E40 to analyze differences in the immune response of four strains of inbred mice (BALB/c, C3H/HeN, 129P2, C57BL/6) after oral infection. The determination of colony-forming units in Peyer's patches and histologic analysis supported the observations that BALB/c are less able to ameliorate the infection within 21 days. The immune defense of C57BL/6 mice against Yersinia was the most effective resulting in a nearly complete elimination of bacteria after 21 days. C3H/HeN and 129P2 were intermediate. Analysis of serum immunoglobulins (Ig) by Luminex showed a significant increase of IgG2b levels 21 days after infection in all four inbred strains. The other immunoglobulins remained nearly constant. Our infection model discriminates between the efficiency of an infection at an early time point (3 days) and immunity at a later time point (21 days). It is furthermore an appropriate model to characterize genetic differences in resistance and immunity of inbred and mutant mouse lines.

Commentary: Missed Opportunities

During the course of economic development, populations have become increasingly urban and geographically mobile. Cities created a new ecology for disease, and colonization brought unfamiliar diseases to colonizers and colonized alike. Urban death rates were usually very much higher than rural ones, and mortality rates from infections were often catastrophically high when new diseases were first introduced to populations. That economic development led to increased rates of urbanization may explain why economic growth rates were sometimes positively correlated with mortality. 11 However, there have also been processes of biological adaptation to the new risks. With new (as distinct from endemic) diseases, people lack the benefit of immunity acquired in early childhood, and selective process have not yet taken their toll of the most genetically susceptible sections of the population. After citing evidence that there were important genetic differences in susceptibility to tuberculosis, Burnett and White 12 gave examples of populations such as American Indians and Mauritians amongst whom it took—largely unaided by economic growth—around a 100 years for mortality rates from TB to fall from initially very high rates to rates as low as Europeans living in similar circumstances. These changes reflect some combination of the benefits of immunity acquired in early life to disease which have become endemic, and a process of genetic selection. Diseases in which there are both genetic differences in resistance, and high death rates before people reach reproductive ages, will tend to remove the most vulnerable sections of the population from the gene pool. Although McKeown and Lowe 3 thought economic growth was

Interactive effects of selection for growth and protein supply on the consequences of gastrointestinal parasitism on growth performance in mice

The consequence of sub-clinical gastrointestinal parasitism in farm animals, i.e. reduced food intake and growth, is often more pronounced in breeds with a high production potential compared with breeds with a low one (Houdijk et al., 2001). It cannot be excluded that such differences in disease resistance may arise from between-breed differences in genetic resistance to parasites rather than production potential per se, as within-breed selected farm animals with sufficiently different production potentials are not readily available. However, appropriately selected mouse lines are available (Bünger et al., 2001) to explore the hypothesis that selection for growth may reduce the animal’s capacity to cope with pathogens. We have recently shown in mice divergently selected for growth potential that in some lines, the absolute penalty of sub-clinical parasitism on high growth mice was higher than in their low growth counterparts (Houdijk and Bünger, 2006). Here, we test the hypothesis that this penalty on growth in one of these lines can be reduced through increased protein supply.

Genetics of disease resistance in sheep and goats

This review summarises the current state of knowledge of the genetic control of resistance to infectious and metabolic diseases in small ruminants. Diseases covered include gastrointestinal nematode infections, diseases due to mycotoxins, bacterial diseases including footrot and mastitis, ectoparasites such as flies and lice, and scrapie, the small ruminant transmissible spongiform encephalopathy. In all cases there is well-documented evidence for between-animal genetic variation in resistance to the disease and, in the case of some of the infectious diseases, resistance to infection. These heritable differences between animals lead to opportunities to breed animals for enhanced resistance to the disease. For some diseases, including nematode parasite infections, resistance to various forms of mycotoxin poisoning and fly-strike, the feasibility of breeding for resistance has been demonstrated in experimental flocks. Importantly, in other cases, including (again) nematode parasite infections and some forms of mycotoxin poisoning, but also mastitis, footrot and scrapie, there are now breeding programmes selecting commercial animals for enhanced resistance. In almost all cases, the evidence for genetic variation and the documented success of breeding for resistance occurs in sheep rather than goats. For nearly all the diseases discussed, there are now concerted efforts to find genetic markers associated with resistance to infection, potentially allowing selection for increased resistance in the absence of infection. Such selection is now implemented for scrapie, as a part of national scrapie eradication programmes, and selection using genetic markers is currently being explored for nematode parasite resistance, footrot resistance and resistance to facial eczema, a mycotoxin poisoning example. Functional genomics, combining gene mapping and gene expression studies, is now being applied to a number of diseases, an example being the identification of genes whose expression underlies genetic differences in resistance to nematode parasites. It is likely that integrated studies combining quantitative and functional genomics, large-scale data collection (both within and between breeds) and epidemiological prediction will lead to new opportunities for breeders to select sheep and goats for enhanced resistance to a variety of diseases.

Genetic Differences in Resistance to Iron Deficiency Chlorosis in Peanut

ABSTRACT Iron (Fe) deficiency has been a widespread problem in peanut (Arachis hypogaea L.) grown on calcareous soils of northern China and has resulted in significant yield losses. Field observations showed considerable variability in visual chlorosis symptoms among peanut cultivars in the same soil. The objective of this study was to confirm the genetic differences in resistance to Fe-deficiency chlorosis in peanut and to identify feasible indicators for screening Fe-efficient genotypes. Resistance to Fe chlorosis of sixteen peanut cultivars grown on calcareous soil was evaluated in the field and physiological responses to Fe-deficiency stress were studied in nutrient solution. There were significant differences in resistance to Fe-deficiency chlorosis among the sixteen peanut cultivars tested, which was identified with SPAD readings, active Fe concentrations in young leaves in the early growth stages, and the pod yield. For Fe-resistant peanut cultivars, Fe-reduction capacity and quality of releasing hydrogen ions from roots increased under Fe-deficiency stress. Highly correlated relationships were observed between the summation of root Fe reduction and field chlorosis scores for sixteen cultivars (r2 = 0.79). It was concluded that Fe-reduction capacity was a better physiological indicator for screening Fe-efficient peanut genotypes of the mechanisms measured.

Lateral plate asymmetry, diet and parasitism in threespine stickleback

Abstract Individuals with random left–right departures from bilateral symmetry are predicted to exhibit fitness reduction including increased parasitism. In an insular lake population of stickleback (Gasterosteus aculeatus) from the Queen Charlotte Islands, Western Canada, phenotypes with high or low number of lateral bony plates exhibited increased plate asymmetry relative to modal phenotypes. Asymmetric lateral plate phenotypes had increased prevalence and to a lesser extent intensity of parasitism relative to symmetric individuals, suggesting that differences in genetic resistance to pathogens contributed to unequal parasitism. The effect occurred mainly in the larger adults and during the warmest season, which may be due to the high metabolic costs incurred during the summer breeding season. Dietary differences between symmetric and asymmetric phenotypes were also detected and could contribute to unequal infection rates by mediating exposure to infected prey items. Our study, which is one of the first long-term field assessments of asymmetry and parasitism, yields results that are consistent with studies linking asymmetry to reduced fitness and indicate that lateral plate asymmetry can be an indicator of poor individual quality, despite its apparent directionality.

Sprout Damage and Preharvest Sprout Resistance in Hard White Winter Wheat

Increased production of hard white winter (HWW) wheat, Triticum aestivum L., in the Great Plains introduces the possibility of preharvest sprouting (PHS) that is often not expressed among widely grown hard red winter (HRW) cultivars. Field experiments were conducted to learn the severity of sprouting likely to occur in contemporary HWW wheat. Specific objectives were to (i) determine the level of sprout damage in Great Plains environments for HWW and HRW genotypes, (ii) assess the level of PHS resistance among the two classes, and (iii) determine the relative merits of germination tests and spike‐wetting treatments. Twenty‐four HWW experimental lines, three HWW cultivars, and five HRW cultivars were evaluated at Stillwater and Lahoma, OK, in 1995 and 1996. Differences in sprout damage measured at two harvest dates were clearly evident between HRW and HWW entries. Pre‐harvest sprout resistance measured at physiological maturity varied widely among HWW lines. No line was as resistant as Plainsman V, a HRW cultivar previously not known to possess high PHS resistance. Two lines were equivalent to the most resistant HWW cultivar, Rio Blanco. Major genes for red kernel color did confer some protection from pre‐harvest sprouting, but their absence did not preclude useful levels of resistance. Chaff tissue played a minor role in influencing genetic differences in resistance. Germination percent at physiological maturity was strongly correlated with field measurements of sprout damage and showed high repeatability. Future improvement of PHS resistance is needed in HWW wheat and should emphasize this component.

Evaluation of major genes affecting resistance to disease in poultry

The results from experimental studies about genetic factors (‘major genes’) involved in disease resistance and their effects in different genetic backgrounds are reviewed and discussed. The major genes considered are (1) Tv-A and Tv-B, gene loci controlling resistance to infection from avian leukosis virus (ALV), (2) B blood groups which represent the major histocompatibility complex (MHC) of the domestic fowl and are indicators of genetic differences in resistance to Marek's disease (MD) and, only tentatively, (3) endogenous viral (ev) genes which can influence reactions to leukosis infection. For these experiments purebred and crossbred progeny from three genetically different experimental White Leghorn lines have been used extensively. The results concerned with leukosis are based on a comparison between groups of chickens which were homozygous resistant or susceptible to ALV infection. The variability in the amount of damage from leukosis points to interactions between the genotype of resistance to ALV infection and genetic characteristics of the line or lines involved. In this respect the negative influence of ev 6 on the immune response to ALV infection could play a role. To study the association of B blood groups and resistance to MD, an experimental line which still segregated at the B locus (B2, B13, B14 and B21) was crossed with two other lines which were homozygous, respectively, for B2 and B15. Mortality caused by MD in birds carrying the same segregating B blood groups showed a completely different pattern in the two crosses. Rather unexpectedly, the difference in MD mortality was largest between the two types of crossbred layers carrying B21, which points to an interaction between line and B blood group type. Further studies suggested that this interaction depends on genes within the MHC for which the lines crossed might differ. The availability of information from different genetic groups allowed an evaluation of the importance of each ‘major gene’ in relation to the comparative effects of other factors influencing the trait under consideration. Apart from becoming aware of possible interactions resulting from genetic differences between lines, simultaneous results from genetically different experimental lines also provide a safeguard against overestimating or underestimating the potential of such ‘major genes’ for practical utilization in poultry breeding.

Deme formation in gall‐making aphids Adelges japonicus (Homoptera: Adelgidae)

AbstractThe deme formation hypothesis in herbivorous insects states that herbivores differentiate genetically into small demes, each specialized in the idiosyncratic traits of individual plants. We examined this hypothesis in gall‐forming aphids, Adelges japonicus, by reciprocal transfers of aphids among three susceptible clones of Picea jezoensis standing in proximity. Performance of aphids transferred to their natal clone was compared with that of aphids transferred to other novel clones. ANCOVA showed no significant donor (source of aphids) by receptor (recipient of aphids) interactions for both total aphid performance on the host tree over a life cycle and its three subdivisions (q1,q2 and q3). In addition, the total performance on the natal clone was lowest among those in the three clones, which was explicitly against the prediction from the local adaptation. In contrast, there were significant receptor effects on q1 (fecundity of gallicolae multiplied by survivorship of fundatrices while feeding on needles) and q3 (fecundity of fundatrices multiplied by survivorship of gallicolae before emergence from the galls), suggesting genetic differences in resistance among clones. The two‐fold difference in q3 among clones was due to different gall size, which was highly correlated with the number of gallicolae that emerged from the gall. The two‐fold difference in q1 seemed to be caused by different survivorship of larval fundatrices while feeding on needles.

A note on the genetics of resistance or susceptibility to ryegrass staggers in sheep

Abstract A flock of mainly Romney × Coopworth ewes was established to test sires for genetic differences in resistance to ryegrass staggers (RGS). This disease is a neurotoxic condition caused by ingestion of endophyte‐infected perennial ryegrass containing the mycotoxin, lolitrem B. Lambs, 18‐month males and females, and ewes of all ages were scored from January to March each year for RGS (0 or 1; 0 = no staggers), while grazing toxic pastures during natural outbreaks of RGS. Over 6 years (the autumns of 1988–93) and over all stock classes scored, age‐group means for RGS ranged from 0 to 0.16. A breeding value for RGS was calculated for each animal, incorporating data from all years and all age groups, provided that the mean year x age group score was at least 0.04. RGS data were also recorded on another Romney flock managed at the same site over the same time period. The heritability of RGS score over both flocks was 0.07 ± 0.02 and the repeatability over years was 0.24 ± 0.04. In March 1993, 170 ewes w...

Effect of water availability on the phenotypic expression of herbivore resistance in northern red oak seedlings (Quercus rubra L.).

The phenotypic expression of quantitative characters is a function of the individual's genotype and the environment in which it is measured. In a previous reciprocal transplant study, we found that patterns of genetic differences in resistance to herbivores among adjacent subpopulations of northern red oak (Quercus rubra L.), were consistent with a local adaptation hypothesis. The goal of this study was to determine if variation in water availability may have been a mechanism responsible for these previously observed patterns. In 1989 a common garden study was initiated using acorns from maternal trees occupying either a north- or south-facing slope microhabitat in an oak-hickory forest in east central Missouri, USA. The seedlings were grown under one of two water treatments, irrigated or natural. In 1992, we utilized this experiment to examine the quantitative character of the percentage of leaf area damaged by herbivores, which is a measure of the phenotypically expressed level of resistance. Specifically, we made three predictions: (1) because northern red oak seem to grow best in mesic environments, seedlings receiving more water should show greater resistance to herbivores; (2) if the subpopulations from north- and south-facing slope microhabitats are genetically differentiated with respect to the quantitative character of resistance to herbivores, then there will be a significant effect of maternal slope microhabitat on the percentage of leaf area damaged; and (3) if the pattern of resistance to herbivores found among subpopulations reflects local adaptation to moisture levels in their own microhabitat, then we would expect to find a significant maternal slope microhabitat by water treatment interaction, with north-facing slope seedlings incurring less damage in the wetter (irrigated) treatment and south-facing slope seedlings incurring less damage in the drier (natural) treatment. Our data supported the first two predictions: seedlings in the irrigated treatment showed a significantly lower percentage of leaf area damage than those in the natural treatment, and the percentage of leaf area damaged was significantly lower on seedlings from maternal plants occupying the north-facing slope microhabitat. However, we found no significant interaction between maternal slope microhabitat and water treatment. These findings demonstrate that northern red oak supbopulations respond phenotypically to water availability, but this factor does not appear to be the underlying mechanism behind the previously observed local adaptation expressed as resistance to herbivores.