Modification of histones immediately following synthesis

The acetylation of newly synthesized histones has been studied by exploiting the ability of sodium butyrate to inhibit deacetylation. Upon arrival in the nucleus a significant fraction of histones H2a, H2b, and H3 is in the parental unmodified form. In contrast histone H4 first appears primarily in the diacetylated form. During an ensuing 135 min the diacetylated H4 is slowly further modified.     

Ablation of the Ferroptosis Inhibitor Glutathione Peroxidase 4 in Neurons Results in Rapid Motor Neuron Degeneration and Paralysis

Glutathione peroxidase 4 (GPX4), an antioxidant defense enzyme active in repairing oxidative damage to lipids, is a key inhibitor of ferroptosis, a non-apoptotic form of cell death involving lipid reactive oxygen species. Here we show that GPX4 is essential for motor neuron health and survival in vivo. Conditional ablation of Gpx4 in neurons of adult mice resulted in rapid onset and progression of paralysis and death. Pathological inspection revealed that the paralyzed mice had a dramatic degeneration of motor neurons in the spinal cord but had no overt neuron degeneration in the cerebral cortex. Consistent with the role of GPX4 as a ferroptosis inhibitor, spinal motor neuron degeneration induced by Gpx4 ablation exhibited features of ferroptosis, including no caspase-3 activation, no TUNEL staining, activation of ERKs, and elevated spinal inflammation. Supplementation with vitamin E, another inhibitor of ferroptosis, delayed the onset of paralysis and death induced by Gpx4 ablation. Also, lipid peroxidation and mitochondrial dysfunction appeared to be involved in ferroptosis of motor neurons induced by Gpx4 ablation. Taken together, the dramatic motor neuron degeneration and paralysis induced by Gpx4 ablation suggest that ferroptosis inhibition by GPX4 is essential for motor neuron health and survival in vivo.     

Differential use of zooplankton prey by Ancient murrelets and Cassin's auklets in the Queen Charlotte Islands

The distribution at sea and the food of two similar sized plankton-feedingalcids were examined during the 1981 breeding seasons in thenorthwestern Queen Charlotte Islands, British Columbia. Thetwo alcids, the Ancient murrelet (Synthliboramphus antiquus)and the Cassin's auklet (Prychoramphus aleuticus) have differentchick-rearing strategies. Both species fed predominantly atthe shelf break, although the Cassin's auklet also foraged overseamounts. The feeding distributions of the species appear tobe related to those of their prey. Zooplankton sampling indicatedthat each alcid selects a small and different portion of thezooplankton available in surface waters. The Ancient murrelet'smain foods were euphausiids (Thysanoessa spinifera and Euphausiapacifica) and larval and juvenile fishes. The Cassin's aukletchicks fed chiefly on calanoid copepods (Neocalanus cristatus).euphausiids (mostly Thysanoessa longipes in 1981, but in otheryears also Thysanoessa spinifera), and larval and juvenile fishes.The Cassin's auklets took smaller prey than the Ancient murrelet.Differences in the diets of the two alcid species were associatedwith differences in morphology and chick-rearing strategies.     

Hosts feeding only Brown‐headed Cowbird fledglings: where are the host fledglings?

ABSTRACT.   Brown-headed Cowbirds ( Molothrus ater ) impose costs on their hosts, usually resulting in fewer or no host young being raised. In 95% of the studies where attempts were made to estimate the cost of parasitism, cost was measured as the difference in host nestling survival in parasitized and unparasitized nests. For hosts that fledge at least some of their own young along with cowbirds, the magnitude of further brood reduction beyond the nestling stage is not known. To examine the possibility that further brood reduction occurs during the fledgling stage, we compiled 102 observations of 45 species feeding fledgling cowbirds. In 97 cases, observers did not record hosts feeding their own young, suggesting that many young die shortly after fledging from parasitized nests. These observations suggest that measuring the cost of parasitism as the difference between the number of host young fledged from parasitized and unparasitized nests probably overestimates the reproductive output of many hosts. If costs increase during the fledgling stage, then the costs of brood parasitism have been underestimated in many studies.