An Arabidopsis jmjC domain protein protects transcribed genes from DNA methylation at CHG sites

Differential cytosine methylation of genes and transposons is important for maintaining integrity of plant genomes. In Arabidopsis, transposons are heavily methylated at both CG and non-CG sites, whereas the non-CG methylation is rarely found in active genes. Our previous genetic analysis suggested that a jmjC domain-containing protein IBM1 (increase in BONSAI methylation 1) prevents ectopic deposition of non-CG methylation, and this process is necessary for normal Arabidopsis development. Here, we directly determined the genomic targets of IBM1 through high-resolution genome-wide analysis of DNA methylation. The ibm1 mutation induced extensive hyper-methylation in thousands of genes. Transposons were unaffected. Notably, long transcribed genes were most severely affected. Methylation of genes is limited to CG sites in wild type, but CHG sites were also methylated in the ibm1 mutant. The ibm1-induced hyper-methylation did not depend on previously characterized components of the RNAi-based DNA methylation machinery. Our results suggest novel transcription-coupled mechanisms to direct genic methylation not only at CG but also at CHG sites. IBM1 prevents the CHG methylation in genes, but not in transposons

Suppression of insertion loss by slit patterning of a magnetic film in a CoFeB/polyimide hybrid thin-film coplanar line for a rf impedance matching device

This article may be downloaded for personal use only. Any other use requires prior permission of the author and the American Institute of Physics. The following article appeared in JOURNAL OF APPLIED PHYSICS. 99(8):08P508 (2006) and may be found at https://doi.org/10.1063/1.2172580 .ArticleJOURNAL OF APPLIED PHYSICS. 99(8):08P508 (2006)journal articl

Mitochondrial retrograde signaling connects respiratory capacity to thermogenic gene expression

Mitochondrial respiration plays a crucial role in determining the metabolic state of brown adipose tissue (BAT), due to its direct roles in thermogenesis, as well as through additional mechanisms. Here, we show that respiration-dependent retrograde signaling from mitochondria to nucleus contributes to genetic and metabolic reprogramming of BAT. In mouse BAT, ablation of LRPPRC (LRP130), a potent regulator of mitochondrial transcription and respiratory capacity, triggers down-regulation of thermogenic genes, promoting a storage phenotype in BAT. This retrograde regulation functions by inhibiting the recruitment of PPARgamma to the regulatory elements of thermogenic genes. Reducing cytosolic Ca2+ reverses the attenuation of thermogenic genes in brown adipocytes with impaired respiratory capacity, while induction of cytosolic Ca2+ is sufficient to attenuate thermogenic gene expression, indicating that cytosolic Ca2+ mediates mitochondria-nucleus crosstalk. Our findings suggest respiratory capacity governs thermogenic gene expression and BAT function via mitochondria-nucleus communication, which in turn leads to either a thermogenic or storage mode

Measuring the Welfare Effects of Slum Improvement Programs: The Case of Mumbai

WP 2007-18 October 2007This paper evaluates the welfare effects of in-situ slum upgrading and relocation programs using data for 5,000 households in Mumbai, India. We estimate a model of residential location choice in which households value the ethnic composition of neighborhoods and employment accessibility in addition to housing characteristics. The importance of neighborhood composition and employment access implies that relocation programs must be designed carefully if they are to be welfare-enhancing. The value of our model is that it allows us to determine the magnitude of these effects. It also allows us to determine the value households place on in situ improvements, which policymakers need to know if they are to design housing programs that permit cost recovery.We thank the World Bank Research Committee and Transport Anchor (TUDTR) for funding the study