Target specificity of mammalian DNA methylation and demethylation machinery.

DNA methylation is an essential epigenetic modification for mammalian embryonic development and biology. The DNA methylation pattern across the genome, together with other epigenetic signals, is responsible for the transcriptional profile of a cell and thus preservation of the cell's identity. Equally, the family of TET enzymes which triggers the initiation of the DNA demethylation cycle plays a vital role in the early embryonic development and a lack of these enzymes at later stages leads to a diseased state and dysregulation of the epigenome. DNA methylation has long been considered a very stable modification; however, it has become increasingly clear that for the establishment and maintenance of the methylation pattern, both generation of DNA methylation and its removal are important, and that a delicate balance of ongoing DNA methylation and demethylation shapes the final epigenetic methylation pattern of the cell. Although this epigenetic mark has been investigated in great detail, it still remains to be fully understood how specific DNA methylation imprints are precisely generated, maintained, read or erased in the genome. Here, we provide a biochemist's view on how both DNA methyltransferases and TET enzymes are recruited to specific genomic loci, and how their chromatin interactions, as well as their intrinsic sequence specificities and molecular mechanisms, contribute to the methylation pattern of the cell.

Changes in the aggressive behavior of cats treated with amphetamine.

Male, adult cats were tested in three different experimental conditions which might lead to aggressive display: (1) Cat-mouse interaction, (2) Predatory competition between two mice killers, (3) Conspecific interactions. DL-amphetamine in a dose of 1.5 mg/kg was administered every day for three weeks to one group of cats, whereas the other group was treated with saline. The following results were observed in amphetamine treated cats: (1) Inhibition or at least a prolonged latency of predatory attack, (2) loss of the dominant status, (3) total lack of offensive behavior and decrease of defensive postures. The results indicate that amphetamine in moderate doses acts to inhibit predatory attack and aggressive behavior in social situations.

The effect of imipramine on predatory behavior and locomotor activity in cats.

The behavior toward mouse was studied under and after chronic imipramine treatment in two groups of cats - non-killers and killers. Imiprarnine facilitated predatory behavior in the non-killers but not in the killers, which is in contrast to results obtained on rats. Imipramine produced a marked decrease of locomotor activity of non-killers tested in open field. The inhibition of locomotion did not interfere with the occurrence of killing behavior. It was concluded that imipramine selectively facilitates the neurophysiological mechanism of predatory behavior, which in cats might be connected with the reward system.