Identification of a major locus conferring resistance to powdery mildew (Erysiphe polygoni DC) in mungbean (Vigna radiata L. Wilczek) by QTL analysis.

A major locus conferring resistance to the causal organism of powdery mildew, Erysiphe polygoni DC, in mungbean (Vigna radiata L. Wilczek) was identified using QTL analysis with a population of 147 recombinant inbred individuals. The population was derived from a cross between 'Berken', a highly susceptible variety, and ATF 3640, a highly resistant line. To test for response to powdery mildew, F7 and F8 lines were inoculated by dispersing decaying mungbean leaves with residual conidia of E. polygoni amongst the young plants to create an artificial epidemic and assayed in a glasshouse facility. To generate a linkage map, 322 RFLP clones were tested against the two parents and 51 of these were selected to screen the mapping population. The 51 probes generated 52 mapped loci, which were used to construct a linkage map spanning 350 cM of the mungbean genome over 10 linkage groups. Using these markers, a single locus was identified that explained up to a maximum of 86% of the total variation in the resistance response to the pathogen.

Development of a mungbean ( Vigna radiata) RFLP linkage map and its comparison with lablab ( Lablab purpureus) reveals a high level of colinearity between the two genomes.

A genetic linkage map of mungbean ( Vigna radiata, 2n = 2 x = 22) consisting of 255 RFLP loci was developed using a recombinant inbred population of 80 individuals. The population was derived from an inter-subspecific cross between the cultivated mungbean variety 'Berken' and a wild mungbean genotype 'ACC 41' ( V. radiata subsp. sublobata). The total length of the map, which comprised 13 linkage groups, spanned 737.9 cM with an average distance between markers of 3.0 cM and a maximum distance between linked markers of 15.4 cM. The mungbean map was compared to a previously published map of lablab ( Lablab purpureus, 2n = 2 x = 24) using a common set of 65 RFLP probes. In contrast to some other comparative mapping studies among members of the Fabaceae, where a high level of chromosomal rearrangement has been observed, marker order between mungbean and lablab was found to be highly conserved. However, the two genomes have apparently accumulated a large number of duplications/deletions after they diverged.

Methane production and energy partition of cattle in the tropics.

The aim of this experiment was to determine CH4 production and energy partition for a range of diets fed to Bos indicus cattle. Six Brahman cattle were fed on three different diets in a replicated Latin square experiment over three periods. The diets were (1) long-chopped Angleton grass (Dicanthium aristatum) hay ad libitum (DM digestibility (DMD) 41 (SE 2)%; 4 g N/kg), (2) long-chopped Rhodes grass (Chloris gayana) hay ad libitum (DMD 60 (SE 1)%; 14 g N/kg) or (3) 2 kg long-chopped lucerne (Medicago sativa) hay/d plus a high-grain diet (ad libitum) (DMD 70 (SE 1)%; 31 g N/kg). CH4 production was measured using confinement-type respiration chambers. Metabolizable energy intake (MJ/d) of cattle fed on Angleton grass (18.4 (SE 2.0)) was lower (P < 0.01) than that for Rhodes grass (54.9 (SE 2.1)), which was lower (P <0.01) than that for the high-grain diet (76.7 (SE 5.8)). CH4 production (g/d) for cattle fed on Rhodes grass (257 (SE 14)) was higher (P < 0.01) than that for cattle fed on both the high-grain diet (160 (SE 24)) and Angleton grass (113 (SE 16)). CH4 conversion rate (MJ CH4 produced per 100 MJ gross energy intake) was not significantly different between cattle fed on Angleton (10.4 (SE 1.1)) and Rhodes (11.4 (SE 0.3)) grass, but was higher (P < 0.01) than for cattle fed on the high-grain diet (6.7 (SE 0.7)). CH4 production (g/kg live-weight gain) was associated (P < 0.001) with both live-weight gain and feed:gain ratio. We conclude that the relationships between CH4 production, energy utilization and live-weight change of cattle fed on tropical forages differ from those of cattle fed on diets based on temperate forages.

Effects of alpha-adrenoceptor agonists and antagonists on metabolic rate in cattle.

Brahman steers (Bos indicus) were treated with the alpha 2-adrenergic agonists, guanfacin.HCl (4-440 micrograms/kg), UK14304.HCl (20-125 micrograms/kg) and clonidine.HCl (0.2-5 micrograms/kg). All three agonists produced dose-dependent reductions in metabolic rate, heart rate and rectal temperature (P < 0.001). Brahman heifers were infused with idazoxan.HCl (10 micrograms/kg/hr), an alpha 2-adrenergic antagonist, alone and in combination with an intramuscular injection of guanfacin.HCl (80 micrograms/kg). Idazoxan alone did not alter rectal temperature but it blocked the guanfacin-induced lowering of rectal temperature (P = 0.05 for the interaction between the two drugs). Idazoxan alone raised metabolic rate (P = 0.01). Guanfacin lowered metabolic rate (P = 0.007) and heart rate (P = 0.03), but the blocking of the guanfacin effect by idazoxan could not be demonstrated (P > 0.05) for either. The same heifers treated with 0.5, 1.0 and 5 micrograms/kg prazosin.HCl, an alpha 1-adrenergic antagonist, had significant changes in metabolic rate (P = 0.003) and heart rate (P = 0.008) at 0.5 and 5 micrograms/kg. Metabolic rate and heart rate decreased at the lower dose and increased at the higher dose. These results with cattle parallel previous results in rats (Gazzola, 1993) where a minimal, conceptual model for the partial control of resting metabolic rate by the sympathetic nervous system was postulated. The model indicates points of control in the sympathetic nervous system which could be manipulated so as to alter the metabolic rate of farm animals.

Growth, nitrogen metabolism, and cardiac responses to clenbuterol and ketoclenbuterol in rats and underfed cattle.

Two beta-adrenoceptor agonists, clenbuterol and ketoclenbuterol, were examined for their effects on growth and cardiac tissue. In female rats, clenbuterol caused a 48% increase in weight gain (P < .05), with improved feed efficiency (26%; P < .1) and increased muscle mass (9%; P < .1). Ketoclenbuterol had less effect on weight gain (30%) and feed efficiency (16%) and did not increase muscle mass. Next we studied the adverse cardiovascular effects of these compounds. Neither drug increased the force of contraction of isolated rat ventricular papillary muscle. Clenbuterol was potent at causing an increase in the rate of contraction of isolated rat atria, and when fed to cattle over 2 d, the drug caused heart rate to increase by 92 to 117%. In contrast, ketoclenbuterol was not a potent stimulator of atrial rate in the rat, and in cattle it caused a smaller increase in heart rate than clenbuterol (12 to 27%). Finally, cattle that were underfed to simulate dry-season tropical pasture conditions were treated with clenbuterol or ketoclenbuterol for 35 d. Ketoclenbuterol caused no beneficial changes in N metabolism. The results obtained with clenbuterol were equivocal, and might have been confounded partly by the refusal of some treated animals to eat all the feed offered. Although clenbuterol did not cause a reduction in total urinary N output relative to control animals, marked reductions in plasma urea concentrations and in urea synthesis were observed (23 to 53%; P < .001). We conclude that ketoclenbuterol is not effective for attenuation of dry-season protein loss in cattle. Clenbuterol seems to be less effective in underfed cattle than in well-fed cattle, and further evidence is required to judge whether compounds of this nature are likely to benefit tropical cattle under harsh grazing conditions.

Effects of guanfacin and nitroprusside on the haemodynamics and oxygen consumption of Brahman steers.

1. The systemic vascular resistance (SVR) and oxygen consumption of high grade Brahman (Bos indicus) steers were measured before and after treatment with guanfacin and nitroprusside to test whether the decreased whole-body oxygen consumption seen with guanfacin treatment is due to less oxygen consumption by vascular smooth muscle. 2. Guanfacin changed oxygen consumption by -31% but raised SVR by 61%. Nitroprusside had no significant effect on oxygen consumption but changed SVR by -20%. Moreover, with guanfacin, the changes in oxygen consumption and SVR were temporally incongruent. 3. We conclude that the lowered whole-body oxygen consumption caused by guanfacin was not due to decreased consumption by vascular tissue.