122 research outputs found

    Characterization of novel microsatellite markers in Musa acuminata subsp. burmannicoides, var. Calcutta 4

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    <p>Abstract</p> <p>Background</p> <p>Banana is a nutritionally important crop across tropical and sub-tropical countries in sub-Saharan Africa, Central and South America and Asia. Although cultivars have evolved from diploid, triploid and tetraploid wild Asian species of <it>Musa acuminata </it>(A genome) and <it>Musa balbisiana </it>(B genome), many of today's commercial cultivars are sterile triploids or diploids, with fruit developing via parthenocarpy. As a result of restricted genetic variation, improvement has been limited, resulting in a crop frequently lacking resistance to pests and disease. Considering the importance of molecular tools to facilitate development of disease resistant genotypes, the objectives of this study were to develop polymorphic microsatellite markers from BAC clone sequences for <it>M. acuminata </it>subsp. <it>burmannicoides</it>, var. Calcutta 4. This wild diploid species is used as a donor cultivar in breeding programs as a source of resistance to diverse biotic stresses.</p> <p>Findings</p> <p>Microsatellite sequences were identified from five Calcutta 4 BAC consensi datasets. Specific primers were designed for 41 loci. Isolated di-nucleotide repeat motifs were the most abundant, followed by tri-nucleotides. From 33 tested loci, 20 displayed polymorphism when screened across 21 diploid <it>M. acuminata </it>accessions, contrasting in resistance to Sigatoka diseases. The number of alleles per SSR locus ranged from two to four, with a total of 56. Six repeat classes were identified, with di-nucleotides the most abundant. Expected heterozygosity values for polymorphic markers ranged from 0.31 to 0.75.</p> <p>Conclusions</p> <p>This is the first report identifying polymorphic microsatellite markers from <it>M. acuminata </it>subsp. <it>burmannicoides</it>, var. Calcutta 4 across accessions contrasting in resistance to Sigatoka diseases. These BAC-derived polymorphic microsatellite markers are a useful resource for banana, applicable for genetic map development, germplasm characterization, evolutionary studies and marker assisted selection for traits.</p

    Emotional over- and under-eating in early childhood are learned not inherited

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    Emotional overeating (EOE) has been associated with increased obesity risk, while emotional undereating (EUE) may be protective. Interestingly, EOE and EUE tend to correlate positively, but it is unclear whether they reflect different aspects of the same underlying trait, or are distinct behaviours with different aetiologies. Data were from 2054 five-year-old children from the Gemini twin birth cohort, including parental ratings of child EOE and EUE using the Child Eating Behaviour Questionnaire. Genetic and environmental influences on variation and covariation in EUE and EOE were established using a bivariate Twin Model. Variation in both behaviours was largely explained by aspects of the environment completely shared by twin pairs (EOE: C = 90%, 95% CI: 89%-92%; EUE: C = 91%, 95% CI: 90%-92%). Genetic influence was low (EOE: A = 7%, 95% CI: 6%-9%; EUE: A = 7%, 95% CI: 6%-9%). EOE and EUE correlated positively (r = 0.43, p < 0.001), and this association was explained by common shared environmental influences (BivC = 45%, 95% CI: 40%-50%). Many of the shared environmental influences underlying EUE and EOE were the same (rC = 0.50, 95% CI: 0.44, 0.55). Childhood EOE and EUE are etiologically distinct. The tendency to eat more or less in response to emotion is learned rather than inherited

    Modelling the Role of the Hsp70/Hsp90 System in the Maintenance of Protein Homeostasis

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    Neurodegeneration is an age-related disorder which is characterised by the accumulation of aggregated protein and neuronal cell death. There are many different neurodegenerative diseases which are classified according to the specific proteins involved and the regions of the brain which are affected. Despite individual differences, there are common mechanisms at the sub-cellular level leading to loss of protein homeostasis. The two central systems in protein homeostasis are the chaperone system, which promotes correct protein folding, and the cellular proteolytic system, which degrades misfolded or damaged proteins. Since these systems and their interactions are very complex, we use mathematical modelling to aid understanding of the processes involved. The model developed in this study focuses on the role of Hsp70 (IPR00103) and Hsp90 (IPR001404) chaperones in preventing both protein aggregation and cell death. Simulations were performed under three different conditions: no stress; transient stress due to an increase in reactive oxygen species; and high stress due to sustained increases in reactive oxygen species. The model predicts that protein homeostasis can be maintained during short periods of stress. However, under long periods of stress, the chaperone system becomes overwhelmed and the probability of cell death pathways being activated increases. Simulations were also run in which cell death mediated by the JNK (P45983) and p38 (Q16539) pathways was inhibited. The model predicts that inhibiting either or both of these pathways may delay cell death but does not stop the aggregation process and that eventually cells die due to aggregated protein inhibiting proteasomal function. This problem can be overcome if the sequestration of aggregated protein into inclusion bodies is enhanced. This model predicts responses to reactive oxygen species-mediated stress that are consistent with currently available experimental data. The model can be used to assess specific interventions to reduce cell death due to impaired protein homeostasis

    Ontogeny of juvenile freshwater pearl mussels, Margaritifera margaritifera (Bivalvia: Margaritiferidae).

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    The gills of juvenile freshwater bivalves undergo a complex morphogenesis that may correlate with changes in feeding ecology, but ontogenic studies on juvenile mussels are rare. Scanning electron microscopy was used to examine the ultrastructure and ontogeny of 117 juvenile freshwater pearl mussels (Margaritifera margaritifera) ranging in age from 1–44 months and length from 0.49–8.90 mm. Three stages of gill development are described. In Stage 1 (5–9 inner demibranch filaments), only unreflected inner demibranch filaments were present. In Stage 2 (9–17 inner demibranch filaments), inner demibranch filaments began to reflect when shell length exceeded 1.13 mm, at 13–16 months old. Reflection began in medial filaments and then proceeded anterior and posterior. In Stage 3 (28–94 inner demibranch filaments), outer demibranch filaments began developing at shell length > 3.1 mm and about 34 months of age. The oral groove on the inner demibranch was first observed in 34 month old specimens > 2.66 mm but was never observed on the outer demibranch. Shell length (R2 = 0.99) was a better predictor of developmental stage compared to age (R2 = 0.84). The full suite of gill ciliation was present on filaments in all stages. Interfilamentary distance averaged 31.3 μm and did not change with age (4–44 months) or with size (0.75–8.9 mm). Distance between laterofrontal cirri couplets averaged 1.54 μm and did not change significantly with size or age. Labial palp primordia were present in even the youngest individuals but ciliature became more diverse in more developed individuals. Information presented here is valuable to captive rearing programmes as it provides insight in to when juveniles may be particularly vulnerable to stressors due to specific ontogenic changes. The data are compared with two other recent studies of Margaritifera development.N/

    Respiratory disease and the role of oral bacteria

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    The relationship between oral health and systemic conditions, including the association between poor oral hygiene, periodontal disease, and respiratory disease, has been increasingly debated over recent decades. A considerable number of hypotheses have sought to explain the possible role of oral bacteria in the pathogenesis of respiratory diseases, and some clinical and epidemiological studies have found results favoring such an association. This review discusses the effect of oral bacteria on respiratory disease, briefly introduces the putative biological mechanisms involved, and the main factors that could contribute to this relationship. It also describes the role of oral care for individuals who are vulnerable to respiratory infections
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