ABSTRACT
The vertebrate kinetochore complex assembles at the centromere on alpha-satellite DNA. In humans, alpha-satellite DNA has a repeat length of 171 bp slightly longer than the DNA in the chromatosome containing the linker histone H1. The centromere-binding protein CENP-B binds specifically to alpha-satellite DNA with properties of a centromeric-linker histone. Here, we analysed if linker histone H1 is present at or excluded from centromeric chromatin by CENP-B. By immunostaining we detected the presence, but no enrichment or depletion of five different H1 subtypes at centromeric chromatin. The binding dynamics of H1 at centromeric sites were similar to that at other locations in the genome. These dynamics did not change in CENP-B depleted cells, suggesting that CENP-B and H1 co-exist in centromeric chromatin with no or little functional overlap. By bimolecular fluorescence complementation (BiFC) and Förster resonance energy transfer (FRET), we revealed that the linker histone H1 subtypes H1 degrees and H1.2 bind to centromeric chromatin in interphase nuclei in direct neighbourhood to inner kinetochore proteins.
Subject(s)
Autoantigens/metabolism , Centromere Protein B/metabolism , Centromere/metabolism , Chromosomal Proteins, Non-Histone/metabolism , Histones/metabolism , Centromere/chemistry , Centromere Protein A , Centromere Protein B/antagonists & inhibitors , Centromere Protein B/genetics , Chromatin/chemistry , Fluorescence Resonance Energy Transfer , HeLa Cells , Histones/analysis , Humans , Kinetochores/metabolism , Microscopy, Fluorescence , RNA InterferenceABSTRACT
A 3-yr study evaluated late winter (Feb), early spring (Apr), and late spring (Jun) calving systems in conjunction with varied weaning strategies on beef cow and calf performance from Northern Great Plains rangelands. Crossbred cows were randomly assigned to one of three calving systems (on average n= 168.calving system(-1).yr(-1)) and one of two weaning times (Wean 1, 2) within each calving system. The Feb and Apr calves were weaned at 190 and 240 d of age, whereas Jun calves were weaned at 140 and 190 d of age. Breeding by natural service occurred in a 32-d period that included estrous synchronization. Cows were managed throughout the year as appropriate for their calving season. Quantity and quality of hay and supplements were provided based on forage and weather conditions, physiological state of the cows, and available harvested feed resources within a year. After weaning, two-thirds of the early weaned steers were fed in confinement in Montana, and one-third were shipped to Oklahoma and were grazed or fed forage. One-half of the early weaned heifers grazed seeded pastures, and the other half was fed in confinement. Early weaned calves were weighed on approximately the same day as late-weaned calves. Birth weight and overall rate of gain from birth to weaning did not differ for calves from the three calving systems. Calf weaning weight differed by weaning age within calving system (P = 0.001), and calves from the Jun calving system that were weaned at 190 d of age tended (P = 0.06) to be lighter than calves of the same age from the Feb or Apr calving systems. Cow BW change and BCS dynamics were affected by calving system, but the proportion of cows pregnant in the fall was not. Cows suckled until later dates gained less or lost more BW during the 50 d between the first and second weaning than dry cows during this period. The previous year's weaning assignment did not affect production in the following year. Estimated harvested feed inputs were less for the Jun cows than for the Feb and Apr cows. We conclude that season of calving and weaning age affect outputs from rangeland-based beef cattle operations.
Subject(s)
Aging , Animal Husbandry/methods , Cattle/growth & development , Weaning , Animal Feed , Animals , Female , Montana , Random Allocation , Seasons , Time Factors , Weather , Weight GainABSTRACT
Coxsackievirus B3 (CVB3) is a common factor in human myocarditis. Apoptotic events are present in CVB3-induced disease, but it is unclear how CVB3 is involved in apoptosis and which viral proteins may induce the apoptotic pathway. In this report we demonstrate that the human and murine proapoptotic protein Siva specifically interact with the CVB3 capsid protein VP2. Furthermore, the transcription of Siva is strongly induced in tissue of CVB3-infected mice and is present in the same area which is positively stained for apoptosis, CD27, and CD70. It has been proposed that Siva is involved in the CD27/CD70-transduced apoptosis. Therefore, we suggest a molecular mechanism through which apoptotic events contributes to CVB3-caused pathogenesis.
