Adsorption and two-body recombination of atomic hydrogen on 3^3He-4^4He mixture films

We present the first systematic measurement of the binding energy $E_a$ of hydrogen atoms to the surface of saturated $^3$He-$^4$He mixture films. $E_a$ is found to decrease almost linearly from 1.14(1) K down to 0.39(1) K, when the population of the ground surface state of $^3$He grows from zero to $6\times10^{14}$ cm$^{-2}$, yielding the value $1.2(1)\times 10^{-15}$ K cm$^2$ for the mean-field parameter of H-$^3$He interaction in 2D. The experiments were carried out with overall $^3$He concentrations ranging from 0.1 ppm to 5 % as well as with commercial and isotopically purified $^4$He at temperatures 70...400 mK. Measuring by ESR the rate constants $K_{aa}$ and $K_{ab}$ for second-order recombination of hydrogen atoms in hyperfine states $a$ and $b$ we find the ratio $K_{ab}/K_{aa}$ to be independent of the $^3$He content and to grow with temperature.Comment: 4 pages, 4 figures, all zipped in a sigle file. Submitted to Phys. Rev. Let

MeCP2 represses the rate of transcriptional initiation of highly methylated long genes.

Mutations in the methyl-DNA-binding repressor protein MeCP2 cause the devastating neurodevelopmental disorder Rett syndrome. It has been challenging to understand how MeCP2 regulates transcription because MeCP2 binds broadly across the genome and MeCP2 mutations are associated with widespread small-magnitude changes in neuronal gene expression. We demonstrate here that MeCP2 represses nascent RNA transcription of highly methylated long genes in the brain through its interaction with the NCoR co-repressor complex. By measuring the rates of transcriptional initiation and elongation directly in the brain, we find that MeCP2 has no measurable effect on transcriptional elongation, but instead represses the rate at which Pol II initiates transcription of highly methylated long genes. These findings suggest a new model of MeCP2 function in which MeCP2 binds broadly across highly methylated regions of DNA, but acts at transcription start sites to attenuate transcriptional initiation