Sources and inheritance of resistance to leaf curl virus in Lycopersicon

Summary One hundred and twenty-two varieties, lines and wild accessions of Lycopersicon were screened under three different regimes during the autumn/winter season of 1982–83 and 1983–84 for resistance to tomato leaf curl virus (TLCV). L. hirsutum f. glabratum (B6013) and L. hirsutum f. typicum (A1904) proved to be highly resistant to TLCV in all three environments. Various accessions of L. peruvianum were also highly resistant. L. pimpinellifolium (A1921) exhibited no TLCV symptoms within 90 days. Of the cultivated varieties, Acc 99 exhibited the minimim score for susceptibility; AC 142, Collection No. 2, Kalyanpur Angurlata and HS 101 had a low rating for virus incidence. The inheritance of resistance was studied in the interspecific crosses between a TLCV resistant line of L. pimpinellifolium (A1921) and five (HS 101, HS 102, HS 110, Pusa Ruby and Punjab Chhuhara) susceptible cultivars of L. esculentum. Parents, F₁, F₂ and backcross progenies were artificially inoculated with local strains of TLCV using vector the viruliferious whitefly, Bemisia tabaci (Genn.). Data indicated that the resistance of L. pimpinellifolium (A 1921) is monogenic and incompletely dominant over susceptibility.     

Inheritance of gynoecism in bitter gourd (Momordica charantia L.)

The inheritance of sex expression in cucumber (Cucumis sativus) and other cucurbits is well documented; however, the genetics of female sex (gynoecism) expression in bitter gourd (Momordica charantia) has not been described. Inheritance of gynoecism in bitter gourd was studied in a 100% gynoecious line (Gy263B). The F(2) and testcross segregation data revealed that gynoecism in Gy263B is under the control of a single, recessive gene. Following the gene nomenclature of cucurbits, it is proposed that the gene symbol, gy-1, be assigned for the expression of gynoecism in bitter gourd.     

Conserved genes act as modifiers of invertebrate SMN loss of function defects

Spinal Muscular Atrophy (SMA) is caused by diminished function of the Survival of Motor Neuron (SMN) protein, but the molecular pathways critical for SMA pathology remain elusive. We have used genetic approaches in invertebrate models to identify conserved SMN loss of function modifier genes. Drosophila melanogaster and Caenorhabditis elegans each have a single gene encoding a protein orthologous to human SMN; diminished function of these invertebrate genes causes lethality and neuromuscular defects. To find genes that modulate SMN function defects across species, two approaches were used. First, a genome-wide RNAi screen for C. elegans SMN modifier genes was undertaken, yielding four genes. Second, we tested the conservation of modifier gene function across species; genes identified in one invertebrate model were tested for function in the other invertebrate model. Drosophila orthologs of two genes, which were identified originally in C. elegans, modified Drosophila SMN loss of function defects. C. elegans orthologs of twelve genes, which were originally identified in a previous Drosophila screen, modified C. elegans SMN loss of function defects. Bioinformatic analysis of the conserved, cross-species, modifier genes suggests that conserved cellular pathways, specifically endocytosis and mRNA regulation, act as critical genetic modifiers of SMN loss of function defects across species.     

Relationship between adiponectin and metabolic variables in Caribbean offspring of patients with type 2 diabetes mellitus.

AIM: To examine the relationship between adiponectin and metabolic variables in the offspring of patients with type 2 diabetes mellitus. METHODS: Fasting blood samples and anthropometric indices were taken from 34 subjects, offspring of patients with type 2 diabetes, and 24 healthy control subjects without any immediate family history of diabetes. Plasma glucose and serum adiponectin, insulin, triglycerides, total cholesterol, HDL and LDL cholesterol levels were measured, and insulin resistance (IR) was calculated based on the homeostasis model assessment (HOMA) method. RESULTS: Offspring and control subjects were sex-matched, but the offspring were older and had higher body mass index and waist circumference than the control subjects (p < 0.05). The offspring had significantly higher mean fasting plasma glucose concentrations; however, their mean serum insulin, adiponectin, triglyceride, total cholesterol, HDL and LDL cholesterol and HOMA-derived IR levels did not significantly differ from those of the control subjects (p > 0.05). While the negative correlation between serum adiponectin and HDL cholesterol levels in the offspring remained statistically significant after adjusting for the effect of age, sex and BMI (r = -0.37, p < 0.05), the negative correlation between adiponectin and serum triglyceride, LDL cholesterol or IR levels became non-significant after controlling for the above variables (p > 0.05 in all cases). CONCLUSION: The correlation between adiponectin and some known biochemical risk factors for developing diabetes and cardiovascular disease in the offspring of patients with diabetes warrants further study to evaluate its potential in assessing the risk of developing these disorders.     

Development of impaired glucose tolerance and diabetes in follow-up offspring of Caribbean patients with type 2 diabetes: analysis of 5-year follow-up study

Several reports agreed that the antecedent markers for developing diabetes in offspring of type 2 diabetic patients involve excess body weight and insulin resistance. This study examined the pattern of changes in anthropometric and biochemical risk factors for developing diabetes in a follow-up offspring of Caribbean type 2 diabetic patients. Results of 46 offspring of type 2 diabetic patients who had received one-to-one individualized diet and exercise counseling for 5 years in our laboratory were analyzed. Changes in anthropometric (body weight, waist circumference) and biochemical (insulin, glucose, lipids, HOMA-insulin resistance, HOMA-percent beta-cell function) parameters over the 5-year period were analyzed using ANOVA tests. Of the 46 offspring, 10.9 and 2.2%, respectively, developed impaired glucose tolerance (IGT) and diabetes. Over the years, IGT offspring had a significant step-wise increase and decrease in fasting and 2-h postprandial plasma glucose levels (P < 0.05) and percent B-cell function (P < 0.001), respectively. Again, a non-significant step-wise increase was observed in body mass index, waist circumference and HOMA-insulin resistance levels (P > 0.05). While we await the results of medication-based intervention studies in different populations, exercise and diet counseling will remain the only available lifestyle intervention strategy for slowing IGT progression to diabetes.