Anti-AKT1 monoclonal antibody, clone 29G20.F6

Transcription factor activation and DNA methylation are important plant responses to abiotic stress. Here, we established that the salinity stress-induced expression of the soybean (Glycine max) transcription factor-encoding gene GmMYB84 relies on DNA methylation. The level of DNA methylation at sequences 690 nt to 950 nt upstream of the GmMYB84 transcription initiation codon was markedly reduced in plants exposed to salinity stress, resulting in a higher abundance of transcripts. When challenged with salinity stress, plants constitutively expressing GmMYB84 outperformed untransformed plants with respect to their germination rate, primary root elongation, proline accumulation, antioxidant enzyme activity, membrane integrity, and K+ levels. Arabidopsis thaliana plants heterologously expressing GmMYB84 were more tolerant to salt stress and exhibited higher germination rates than the wild type. Electrophoretic mobility shift assays revealed that GmMYB84 binds to the cis-regulatory sequences of GmAKT1, the homolog of ARABIDOPSIS K+ TRANSPORTER 1 (AKT1). Thus, DNA methylation modulates the salinity stress-induced expression of the soybean transcription factor-encoding gene GmMYB84 and thereby confers salinity stress tolerance.

Purpose Proteus syndrome arises as a result of a post-zygotic mosaic activating mutation in the AKT1 oncogene, causing a disproportionate overgrowth of affected tissues. A small number of ocular complications have been reported. We present the unique findings in a patient who had molecular confirmation of AKT1 mosaicism alongside fulfilling the clinical criteria for Proteus syndrome. Methods Pattern electroretinography, visual evoked potentials and multifocal electroretinography testing were performed alongside detailed retinal imaging and clinical examination to detail the ophthalmic characteristics. Results Electrophysiological findings characterised unilateral macular dysfunction alongside sector retinal dysfunction of the right eye. This was demonstrated through optical coherence tomography and ultra-wide-field imaging to be associated with a misaligned foveal morphology and sector retinal dysfunction extending into the temporal retina. Conclusion We propose this patient has asymmetric foveal development and concomitant sector retinal dysfunction as the result of the mosaic AKT1 mutation, either through disruption in the retinal PI3K-AKT1 signalling pathway or through mechanical distortion of ocular growth, resulting in disproportionate inner retinal development. The findings expand the ocular phenotype of Proteus syndrome and encourage early assessment to identify any incipient ocular abnormalities.