Abstracts of papers presented at the fifteenth Genetics Society's Mammalian Genetics and Development Workshop held at the Institute of Child Health, University College London on 22 and 23 November 2004.
The Transforming growth factor-beta (TGF-beta) family control diverse cellular processes and specify cell-fate/differentiation during embryogenesis in vertebrates and invertebrates. Mutations disrupting TGF-beta signalling lead to developmental abnormalities and a range of diseases such as cancer. Nodal is a major TGF-beta signal, responsible for gastrulation in embryogenesis. Arkadia ( Akd) was discovered by mouse gene-trap mutagenesis and encodes a nuclear E3 ubiquitin ligase. Akd allows the Nodal signal to reach its maximum level and Akd-null mice lack mammalian organiser (MO) and mesendodermal tissues. Although Akd RNA is ubiquitously expressed, Akd-null mice lose a subset of Nodal-dependent functions. The specificity of Akd function is therefore most likely to be regulated post-transcriptionally or by co-factors. Akd possesses differentially spliced 5' untranslated regions (UTRs) and large 3' UTR. We have employed bioinformatics and developed a reporter system to address Akd post-transcriptional regulation. Akd RNA may initiate from different promoters and 5' UTR differential splicing, upstream AUGs (uAUGs) and open-reading frames upstream (uORFs) may regulate protein translation. 5' and 3' UTRs can interact to either destabilise or decrease translational efficiency of RNA. The nature of this interaction is cell-type and signal level dependent. These data may represent mechanisms by which translational control of Arkadia is achieved and ultimately how TGF-beta/ Nodal signalling is regulated during embryogenesis.[1]References
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