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Abstract: Frataxin is present in mitochondria of all eukaryotes as well as in the cytoplasm of bacteria. In humans, reduced expression of frataxin is associated with Friedreich’s ataxia, a recessive inherited neurodegenerative and cardiac disorder leading to reduced life expectancy. Experimental evidences suggest that frataxin acts as an iron-chaperone protein, donating iron to the proteins involved in [Fe–S] cluster assembly and heme synthesis. It also possibly contributes to the process of iron detoxification and storage. The frataxin homolog from Arabidopsis thaliana (AtFH) is a single nuclear-encoded gene targeted to mitochondria and sharing 65% similarity with animal frataxin. In the present work, we show that the knocking out of AtFH gene causes arrest of Arabidopsis embryo development at the globular stage. Consistently with that, we also show by in situ hybridization that AtFH is expressed, in wt Arabidopsis plants, in ovule primordia as well as in embryos at various stages of development, suggesting a key role of plant frataxin during embryogenesis. [Copyright &y& Elsevier]

The mechanisms for the regulation of homeotic genes are poorly understood in most organisms, including plants. We identified BASIC PENTACYSTEINE1 (BPC1) as a regulator of the homeotic Arabidopsis thaliana gene SEEDSTICK (STK), which controls ovule identity, and characterized its mechanism of action. A combination of tethered particle motion analysis and electromobility shift assays revealed that BPC1 is able to induce conformational changes by cooperative binding to purine-rich elements present in the STK regulatory sequence. Analysis of STK expression in the bpcl mutant showed that STK is upregulated. Our results give insight into the regulation of gene expression in plants and provide the basis for further studies to understand the mechanisms that control ovule identity in Arabidopsis. [ABSTRACT FROM AUTHOR]