BackgroundProduction of cassava (Manihot esculenta Crantz), a food security crop in sub-Saharan Africa, is threatened by the spread of cassava brown streak disease (CBSD) which manifests in part as a corky necrosis in the storage root. It is caused by either of two virus species, Cassava brown streak virus (CBSV) and Ugandan cassava brown streak virus (UCBSV), resulting in up to 100% yield loss in susceptible varieties.MethodsThis study characterized the response of 11 cassava varieties according to CBSD symptom expression and relative CBSV and UCBSV load in a field trial in Uganda. Relative viral load was measured using quantitative RT-PCR using COX as an internal housekeeping gene.ResultsA complex situation was revealed with indications of different resistance mechanisms that restrict virus accumulation and symptom expression. Four response categories were defined. Symptom expression was not always positively correlated with virus load. Substantially different levels of the virus species were found in many genotypes suggesting either resistance to one virus species or the other, or some form of interaction, antagonism or competition between virus species.ConclusionsA substantial amount of research still needs to be undertaken to fully understand the mechanism and genetic bases of resistance. This information will be useful in informing breeding strategies and restricting virus spread.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-014-0216-x) contains supplementary material, which is available to authorized users.
Cassava (Manihot esculenta Crantz) production is currently under threat from cassava brown streak disease (CBSD), a disease that is among the seven most serious obstacles to world’s food security. Three issues are of significance for CBSD. Firstly, the virus associated with CBSD, has co-evolved with cassava outside its center of origin for at least 90 years. Secondly, that for the last 74 years, CBSD was only limited to the low lands. Thirdly, that most research has largely focused on CBSD epidemiology and virus diversity. Accordingly, this paper focuses on CBSD genetics and/or breeding and hence, presents empirical data generated in the past 11 years of cassava breeding in Uganda. Specifically, this paper provides: 1) empirical data on CBSD resistance screening efforts to identify sources of resistance and/or tolerance; 2) an update on CBSD resistance population development comprising of full-sibs, half-sibs and S1 families and their respective field performances; and 3) insights into chromosomal regions and genes involved in CBSD resistance based on genome wide association analysis. It is expected that this information will provide a foundation for harmonizing on-going CBSD breeding efforts and consequently, inform the future breeding interventions aimed at combating CBSD.
Cassava brown streak disease (CBSD) caused by Cassava brown streak virus (CBSV) and Ugandan cassava brown streak virus (UCBSV) is a threat to food security in sub-Saharan Africa, where the disease persistently reduces overall root quality and quantity resulting in up to 100% yield losses. Complexities in CBSD symptom expression and the damage caused on leaves, stems and roots throughout the 12 months of cassava growth require that appropriate ways of categorizing genotype response and optimal stages of evaluation be identified. This study aimed at: 1) determining plot based heritability of CBSD based on symptom expression and 2) categorizing genotype resistance to CBSD based on symptom expression. Herein, 41 genotypes were evaluated for two years at Namulonge with an additional evaluation conducted across three locations. Evaluations were done at three, six, nine and twelve months after planting. Genotype responses to CBSD varied significantly. High broad sense heritability estimates of up to 0.81 (incidence) and 0.71 (severity) were obtained.Average disease severity scores had higher broad sense heritability estimates (0.53 and 0.65) than maximum disease severity scores (0.33 and 0.61) for root and foliar severities respectively. These findings are important in choosing an appropriate evaluation method for CBSD. Genotypes displayed differing CBSD responses in type, locality and severity of symptoms. This suggested that genotypes had differences in mechanisms of resistance that can be exploited in CBSD resistance breeding.
Insects feeding on the nutrient-poor diet of xylem plant sap generally bear two microbial symbionts that are localized to different organs (bacteriomes) and provide complementary sets of essential amino acids (EAAs). Here, we investigate the metabolic basis for the apparent paradox that xylem-feeding insects are under intense selection for metabolic efficiency but incur the cost of maintaining two symbionts for functions mediated by one symbiont in other associations. Using stable isotope analysis of central carbon metabolism and metabolic modeling, we provide evidence that the bacteriomes of the spittlebug Clastoptera proteus display high rates of aerobic glycolysis, with syntrophic splitting of glucose oxidation. Specifically, our data suggest that one bacteriome (containing the bacterium Sulcia, which synthesizes seven EAAs) predominantly processes glucose glycolytically, producing pyruvate and lactate, and the exported pyruvate and lactate is assimilated by the second bacteriome (containing the bacterium Zinderia, which synthesizes three energetically costly EAAs) and channeled through the TCA cycle for energy generation by oxidative phosphorylation. We, furthermore, calculate that this metabolic arrangement supports the high ATP demand in Zinderia bacteriomes for Zinderia-mediated synthesis of energy-intensive EAAs. We predict that metabolite cross-feeding among host cells may be widespread in animal–microbe symbioses utilizing low-nutrient diets.
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