Resistance of potato clones to the green peach aphid and potato leafroll virus

During 1980 and 1981 potato cultivars and breeding selections, including cultivated species and their hybrid derivatives, were evaluated for resistance to the green peach aphid (GPA),Myzus persicae (Sulzer), and to potato leafroll virus (PLRV). Criteria used were the number of aphids which colonized the clones in free choice field experiments and the number of plants derived from these experiments which showed symptoms of PLRV infection. Generally, greater resistance to GPA was found inSolarium tuberosum gp.andigena selections and hybrids than in gp.tuberosum cultivars. There were approximately fourfold differences in season-mean GPA levels among the clones tested each year. Forty-two families, representing a cross-section of the USDA breeding populations at the University of Idaho Research and Extension Center, Aberdeen, showed a similar range in colonization levels. Resistance to GPA colonization appeared to be more prevalent in gp.andigena, gp.phureja, and gp.stenotonum derivatives. There was a weak positive correlation (r² = .34, P = .01) between foliar total glycoalkaloids and season-mean GPA colonization levels for six clones representing the range of observed resistance to GPA. Resistance to GPA colonization was apparently not directly related to resistance to PLRV infection. Katahdin, for example, was relatively susceptible to GPA colonization but very resistant to PLRV infection whereas selection A69657-4 (gp.andigena) was among the most resistant to GPA colonization but among the more susceptible to PLRV infection. Breeding for resistance to GPA colonization therefore may not be as promising for PLRV control as developing PLRV resistant cultivars.     

Genetic parameters for performance traits in commercial sows estimated before and after an outbreak of porcine reproductive and respiratory syndrome

Porcine reproductive and respiratory syndrome (PRRS), caused by the PRRS virus (PRRSV), is globally the most economically important disease in commercial pigs, and novel control strategies are sought. This paper explores the potential to use host genetics to decrease the impact of PRRS on reproductive sows. Commercial pig data (7,542 phenotypic records) from a farm undergoing an outbreak of PRRSV were analyzed to assess the impact of PRRS on reproductive traits and the inheritance of such traits. First, differing methodologies were used to partition the data into time periods when the farm was disease free and when the farm was experiencing PRRSV outbreaks. The methods were a date/threshold method based on veterinary diagnosis and a threshold/threshold method based on trends in underlying performance data, creating the DTD and TTD data sets, respectively. The threshold/threshold method was more stringent in defining periods when PRRS was likely to be having an impact on reproductive performance, resulting in a data set (TTD) that was slightly smaller (1,977 litters from 1,526 sows) than that from the date/threshold method (3,164 litters and 1,662 sows), and it showed more pronounced impacts of PRRS on performance. Impacts on performance included significant increases in mean values of mummified and stillborn piglets (0.04 to 1.13 and 0.63 to 1.02, respectively) with a significant decrease in total born alive (10.3 to 9.08). Estimated heritabilities during the healthy phase were generally less (mummified piglets = 0.03 +/- 0.01, matings per conception = 0.04 +/- 0.01) than during the PRRSV outbreak (TTD data set; mummified piglets = 0.10 +/- 0.03, matings per conception = 0.46 +/- 0.04). These results imply genetic variation for host resistance to, or tolerance of, PRRSV, particularly with the TTD data set. Genetic correlations between reproductive traits measured in the healthy phase and TTD data set varied from effectively zero for traits describing numbers of mummified or dead piglets to strongly positive for litter size traits. This indicates genetic variation in piglet losses during PRRSV outbreaks is independent of genetic variation in the same traits in healthy herds. In summary, our findings show that there is within-breed genetic variation for commercially relevant traits that could be exploited in future breeding programs against PRRSV infection. Selection for increased PRRS resistance would be desirable to the industry because effective control measures remain elusive.     

A Non‐Reciprocal Autosomal Translocation 64,XX,t(4;10)(q21;p15) in an Arabian Mare with Repeated Early Embryonic Loss

Balanced autosomal translocations are a known cause for repeated early embryonic loss (REEL) in horses. In most cases, carriers of such translocations are phenotypically normal, but the chromosomal aberration negatively affects gametogenesis giving rise to both genetically balanced and unbalanced gametes. The latter, if involved in fertilization, result in REEL, whereas gametes with the balanced form of translocation will pass the defect into next generation. Therefore, in order to reduce the incidence of REEL, identification of translocation carriers is critical. Here, we report about a phenotypically normal 3‐year‐old Arabian mare that had repeated resorption of conceptuses prior to day 45 of gestation and was diagnosed with REEL. Conventional and molecular cytogenetic analyses revealed that the mare had normal chromosome number 64,XX but carried a non‐mosaic and non‐reciprocal autosomal translocation t(4;10)(q21;p15). This is a novel translocation described in horses with REEL and the first such report in Arabians. Previous cases of REEL due to autosomal translocations have exclusively involved Thoroughbreds. The findings underscore the importance of routine cytogenetic screening of breeding animals.