How a mismatch repair enzyme balances the needs for efficient lesion processing and minimal action on undamaged DNA

Comment on: Maiti A, et al. Proc Natl Acad Sci USA 2012; 109:8091-6.     

Reciprocal allopolyploid grasses (Festuca × Lolium) display stable patterns of genome dominance

Allopolyploidization entailing the merger of two distinct genomes in a single hybrid organism, is an important process in plant evolution and a valuable tool in breeding programs. Newly established hybrids often experience massive genomic perturbations, including karyotype reshuffling and gene expression modifications. These phenomena may be asymmetric with respect to the two progenitors, with one of the parental genomes being “dominant.” Such “genome dominance” can manifest in several ways, including biased homoeolog gene expression and expression level dominance. Here we employed a k-mer–based approach to study gene expression in reciprocal Festuca pratensis Huds. × Lolium multiflorum Lam. allopolyploid grasses. Our study revealed significantly more genes where expression mimicked that of the Lolium parent compared with the Festuca parent. This genome dominance was heritable to successive generation and its direction was only slightly modified by environmental conditions and plant age. Our results suggest that Lolium genome dominance was at least partially caused by its more efficient trans-acting gene expression regulatory factors. Unraveling the mechanisms responsible for propagation of parent-specific traits in hybrid crops contributes to our understanding of allopolyploid genome evolution and opens a way to targeted breeding strategies.     

Mechanisms of cell division as regulators of acute immune response

The acute adaptive immune response is complex, proceeding through phases of activation of quiescent lymphocytes, rapid expansion by cell division and cell differentiation, cessation of division and eventual death of greater than 95 % of the newly generated population. Control of the response is not central but appears to operate as a distributed process where global patterns reliably emerge as a result of collective behaviour of a large number of autonomous cells. In this review, we highlight evidence that competing intracellular timed processes underlie the distribution of individual fates and control cell proliferation, cessation and loss. These principles can be captured in a mathematical model to illustrate consistency with previously published experimentally observed data.     

Posttranscriptional Regulation by the Upstream Open Reading Frame of the Phosphoethanolamine N-Methyltransferase Gene

Phosphoethanolamine N-methyltransferase (PEAMT) is involved in choline biosynthesis in plants. The 5′ untranslated region (UTR) of several PEAMT genes was found to contain an upstream open reading frame (uORF). We generated transgenic Arabidopsis calli that expressed a chimeric gene constructed by fusing the 5′ UTR of the Arabidopsis PEAMT gene (AtNMT1) upstream of the β-glucuronidase gene. The AtNMT1 uORF was found to be involved in declining levels of the chimeric gene mRNA and repression of downstream β-glucuronidase gene translation in the calli when the cells were treated with choline. Further, we discuss the role of the uORF.     

Molecular Co-occupancy Identifies Transcription Factor Binding Cooperativity In Vivo

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A unique histone 3 lysine 14 chromatin signature underlies tissue-specific gene regulation

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Biphasic Regulation in Ligand-Receptor Interactions

Abstract

A model is examined in which an excess of activator may inhibit the response in a ligand-receptor interaction. The equation accounts for biphasic responses in which an effector stimulates the response at low concentrations and then inhibits the response at higher concentrations, towards a limit that can be higher, identical or lower than the initial value. Reciprocal features could be observed according to the values of the involved parameters. A maximum 7 dimensions can be found in the space of the parameters of the equation which is of the simple form: v = (A + B + C). Sⁿ/(H + Sⁿ).