Embryology Research Today is a free monthly online journal that collates and summarizes the latest research about Embryology, including details on stem cells, reproduction, transplants, cloning.

Knockout of frataxin gene causes embryo lethality in Arabidopsis.

Vazzola V, Losa A, Soave C, Murgia I

Sezione di Fisiologia e Biochimica delle Piante, Dipartimento di Biologia, Università degli Studi di Milano, via Celoria 26, 20133 Milano, Italy.

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.

Published 13 February 2007 in FEBS Lett, 581(4): 667-72.
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