Characterization of constricted fruit (ctf) Mutant Uncovers a Role for AtMYB117/LOF1 in Ovule and Fruit Development in Arabidopsis thaliana

Pistil and fruit morphogenesis is the result of a complex gene network that is not yet fully understood. A search for novel genes is needed to make a more comprehensive model of pistil and fruit development. Screening for mutants with alterations in fruit morphology generated by an activation tagging strategy resulted in the isolation of the ctf (constricted fruit) mutant. It is characterized by a) small and wrinkled fruits, with an enlarged replum, an amorphous structure of the septum and an irregular distribution of ovules and seeds; b) ectopic carpelloid structures in sepals bearing ovule-like structures and c) dwarf plants with curled rosette leaves. The overexpressed gene in ctf was AtMYB117, also named LOF1 (LATERAL ORGAN FUSION1). AtMYB117/LOF1 transcripts were localized in boundary regions of the vegetative shoot apical meristem and leaf primordia and in a group of cells in the adaxial base of petioles and bracts. Transcripts were also detected in the boundaries between each of the four floral whorls and during pistil development in the inner of the medial ridges, the placenta, the base of the ovule primordia, the epidermis of the developing septum and the outer cell layers of the ovule funiculi. Analysis of changes of expression of pistil-related genes in the ctf mutant showed an enhancement of SHATTERPROOF1 (SHP1) and SHP2 expression. All these results suggest that AtMYB117/LOF1 is recruited by a variety of developmental programs for the establishment of boundary regions, including the development of floral organs and the initiation of ovule outgrowth

Altered gene expression and DNA damage in peripheral blood cells from Friedreich's ataxia patients: Cellular model of pathology

The neurodegenerative disease Friedreich's ataxia (FRDA) is the most common autosomal-recessively inherited ataxia and is caused by a GAA triplet repeat expansion in the first intron of the frataxin gene. In this disease, transcription of frataxin, a mitochondrial protein involved in iron homeostasis, is impaired, resulting in a significant reduction in mRNA and protein levels. Global gene expression analysis was performed in peripheral blood samples from FRDA patients as compared to controls, which suggested altered expression patterns pertaining to genotoxic stress. We then confirmed the presence of genotoxic DNA damage by using a gene-specific quantitative PCR assay and discovered an increase in both mitochondrial and nuclear DNA damage in the blood of these patients (p<0.0001, respectively). Additionally, frataxin mRNA levels correlated with age of onset of disease and displayed unique sets of gene alterations involved in immune response, oxidative phosphorylation, and protein synthesis. Many of the key pathways observed by transcription profiling were downregulated, and we believe these data suggest that patients with prolonged frataxin deficiency undergo a systemic survival response to chronic genotoxic stress and consequent DNA damage detectable in blood. In conclusion, our results yield insight into the nature and progression of FRDA, as well as possible therapeutic approaches. Furthermore, the identification of potential biomarkers, including the DNA damage found in peripheral blood, may have predictive value in future clinical trials

Electronic properties of monolayer and bilayer graphene

The tight-binding model of electrons in graphene is reviewed. We derive low-energy Hamiltonians supporting massless Dirac-like chiral fermions and massive chiral fermions in monolayer and bilayer graphene, respectively, and we describe how their chirality is manifest in the sequencing of plateaus observed in the integer quantum Hall effect. The opening of a tuneable band gap in bilayer graphene in response to a transverse electric field is described, and we explain how Hartree theory may be used to develop a simple analytical model of screening