The impact of respiratory disease during a 150-d feedlot finishing period on daily gain, carcass traits, and longissimus tenderness was measured using 204 steer calves. Feedlot health status was monitored in two ways. First, clinical signs of respiratory infection were evaluated each day; treatment with antibiotic was based on degree of fever (if rectal temperature exceeded 40 degrees C then calves were treated). Steers that were treated (n = 102) had lower (P<.05) final live weights, ADG, hot carcass weights (HCW), less external and internal fat, and more desirable yield grades. Steers that were treated had a higher prevalence of carcasses that graded U.S. Standard than steers that were never treated. Second, as an alternative index of health status, lungs of all steers were evaluated at the processing plant using a respiratory tract lesion classification system; this health index included presence or absence of preexisting pneumonic lesions in the anterioventral lobes plus activity of the bronchial lymph nodes (inactive vs active). Lung lesions were present in 33% of all lungs and were distributed almost equally between treated (37%) and untreated cattle (29%). Steers with lesions (n = 87) had lower (P<.05) daily gains, lighter HCW, less internal fat, and lower marbling scores than steers without lesions. Compared to steers with lesions but inactive bronchial lymph nodes (n = 78), steers with lung lesions plus active lymph nodes had lower (P<.01) ADG and dressing percentage. Longissimus shear force values for steaks aged 7 d were lower (P = .05) from steers without lung lesions than those for steaks from steers with lung lesions. Overall, morbidity suppressed daily gains and increased the percentage of U.S. Standard carcasses. Compared to health assessment by clinical appraisal (based on elevated body temperature), classification based on respiratory tract lesions at slaughter proved more reliable statistically and, thereby, more predictive of adverse effects of morbidity on production and meat tenderness.
Cells rely on a network of conserved pathways to govern DNA replication fidelity. Loss of polymerase proofreading or mismatch repair elevates spontaneous mutation and facilitates cellular adaptation. However, double mutants are inviable, suggesting that extreme mutation rates exceed an error threshold. Here we combine alleles that affect DNA polymerase δ (Pol δ) proofreading and mismatch repair to define the maximal error rate in haploid yeast and to characterize genetic suppressors of mutator phenotypes. We show that populations tolerate mutation rates 1,000-fold above wild-type levels but collapse when the rate exceeds 10−3 inactivating mutations per gene per cell division. Variants that escape this error-induced extinction (eex) rapidly emerge from mutator clones. One-third of the escape mutants result from second-site changes in Pol δ that suppress the proofreading-deficient phenotype, while two-thirds are extragenic. The structural locations of the Pol δ changes suggest multiple antimutator mechanisms. Our studies reveal the transient nature of eukaryotic mutators and show that mutator phenotypes are readily suppressed by genetic adaptation. This has implications for the role of mutator phenotypes in cancer.
Morbidity and mortality of feedlot cattle have a variety of causes. Compared to respiratory disease, metabolic and digestive disorders generally are less prevalent and occur later in the feeding period. In addition to the obvious costs related to animal death and medication, subsequent performance of sick cattle often is depressed substantially. Closer coordination between veterinarians, nutritionists, and feedlot managers should help reduce the incidence of morbidity and mortality of feedlot cattle.
The cheA locus of Escherichia coli, which is required for chemotactic behavior, encodes two polep tide products designated p[cheA]L and pjcheA]s. The mode of synthesis of these two proteins was investigated b transferring various missense and nonsense mutations to a A transducing phage and observing the mutant cheA products made after infection of ultraviolet-irradiated host cells. Missense mutations had no effect on either the size or the relative amounts of the two cheA polypeptides. Overlapping genes, which synthesize more than one polypeptide product from the same coding sequence, have been observed in a number of bacterial and animal viruses. Some overlapping gene pairs in bacteriophage-for example, A and A* in 4X174 or C and Nu3 in X-are transcribed from a common promoter and translated in the same reading frame, but from different initiation sites, yielding two related proteins (1, 2). The A1 and coat proteins of phage QB are also translated in the same phase but differ at their carboxyl ends due to an inefficient translation termination signal (3). Other overlapping genes in bacteriophages OX174 and G4 are transcribed from independent promoters and then translated in different reading frames, yielding essentially unrelated products from the same coding sequence (4,5). Animal viruses such as polyoma virus and simian virus 40 utilize messenger RNA splicing to synthesize several proteins, either in the same or different reading frames, from one coding sequence (6, 7).Regardless of their mechanism of expression, overlapping genes are generally thought to have evolved as a means of increasing the coding capacity of viral genomes without a concomitant increase in overall genorne size, which in most viruses is limited by the capacity of the virion. According to this view, the evolutionary constraints that accompany the use of the same nucleotide sequence by two different genes are offset by selective pressures to retain a particular genome size. If this were the only factor favoring the existence of overlapping genes, it seems unlikely they would have arisen in bacteria or higher cells, in which limitations on the amount of genetic material are much less severe than in viruses.In this report we describe an apparent case of overlapping genes at the cheA locus in Escherichia colh. Mutants defective in cheA function are viable but nonchemotactib due to an inability to change directions as they swim (8, 9). Silverman, Simon, and coworkers (10, 11) constructed X phages carrying the cheA region and showed that cheA complementation activity was associated with the presence of two polypeptides.t In order to determine the nature of the relationship between these two cheA products, we examined the functional properties and the polypeptide products of a variety of cheA mutants. Our findings are consistent with a model in which both polypeptides are translated independently from the same coding sequence and in the same reading frame, but from different initiation sites. Moreover, each polypeptide may have a distin...
Secretion of calf prochymosin from yeast yields fully activable zymogen while production in the yeast cytoplasm yields insoluble, unactivable enzyme with aberrant disulfide bonding. Factors that increase the efficiency of secretion of prochymosin from yeast are use of a yeast secretion signal sequence, integration of the transcriptional unit into the yeast genome, and specific mutations in a number of host cell genes. In combination, these factors increase the secretion of calf prochymosin from less than 1 percent to more than 80 percent of the amount produced. Host mutations that increase prochymosin secretion also increase bovine growth hormone secretion more than 15-fold. These discoveries may be generally useful for production of many secreted mammalian proteins made inside microorganisms as insoluble aggregates.
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