| For investigation of genetic mechanisms of leaf polarity formation, we screened for Arabidopsis mutants with aberrant leaf morphology by ethylmethane sulfonate (EMS) mutagenesis. Among leaf mutants we have obtained, 7 independent lines showed very similar leaf phenotypes to each other: some of the first pair rosette leaves with petiole growth from underneath leaf blade, displaying a lotus-leaf structure. Allelism tests revealed that these phenotype-similar mutants could be divided into two complementary groups that were named ll1 and ll2 (for lotus leaves), respectively. In addition to the lotus-leaf phenotype, other leaves were also similar to those of the previously reported mutants, asymmetric leaves1 (as1) and asymmetric leaves2 (as2). We therefore also performed allelism tests between ll and as mutants. Our results show that ll1 is the as2 mutant, and ll2 is the as1 mutant. I have cloned the AS1 gene by map-based cloning. The sequence analysis revealed that the AS1 gene encodes a MYB protein, which is a candidate transcription factor. In as1 and as2 mutants, the polarity formation in leaves is defective. Cell differentiation along abaxial-adaxial, proximal-distal and media-lateral axes all shows an insufficient fashion. Leaf primordia of the as1-101 and as2-101 mutants grew slowly in comparison to those in wild-type. The AS1 and AS2 genes expressed with a similar pattern in the wild-type plants. They express strongly in young leaves and flowers. RT-PCR results showed that there are no substantial changes in expression levels when AS1 expressed in the as2 mutant, or AS2 expressed in the as1 mutant, indicating a direct transcriptional regulation between these two genes is not likely. We also provide strong evidence to show that the more severe phenotypes in the newly isolated as1 and as2 mutants result from the Ler genetic background.
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