ORCID Profile
0000-0001-9000-7502
Current Organisation
Kumamoto University
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Publisher: Oxford University Press (OUP)
Date: 04-2010
DOI: 10.1093/PCP/PCQ028
Abstract: The shoot meristem is a group of self-perpetuating cells that ultimately gives rise to the aerial parts of plants. The Arabidopsis thaliana SHOOT MERISTEMLESS (STM) gene, which encodes a knotted1-like homeobox transcription factor, is required for shoot meristem formation and maintenance, and loss-of-function mutations in the gene result in complete loss or premature termination of the shoot meristem. Here, we report a novel missense allele of STM, gorgon (gor), which displays striking differences in shoot meristem defects compared with known stm alleles. The gor phenotype results from substitution of the highly conserved arginine at position 53 of the homeodomain, which is important for DNA binding in other homeodomain proteins. In gor, the shoot meristem enlarges continuously during post-embryonic development and the floral meristems frequently develop additional whorls. These phenotypes, together with enlarged expression domains of meristem markers, indicate that the mutation affects shoot meristem activity in the opposite direction to other loss-of-function alleles. However, detailed genetic analyses and overexpression studies indicate that gor represents a novel type of hypomorphic alleles rather than the hypermorph that is suggested by the phenotype. Consistently, the gor allele strictly requires the functional PENNYWISE (PNY) gene, which encodes a known binding partner of the STM protein, to maintain shoot meristem activity, whereas the wild-type allele efficiently maintains the meristem even in the absence of PNY. Our results suggest a critical role for Arg53 of the homeodomain in STM function and that the gor mutation at this residue impairs shoot meristem homeostasis.
Publisher: Oxford University Press (OUP)
Date: 10-2008
Abstract: Seed morphogenesis consists of embryogenesis and the development of maternal tissues such as the inner and outer integuments, both of which give rise to seed coats. We show that expression of chimeric repressors derived from NAC-REGULATED SEED MORPHOLOGY1 and -2 (NARS1 and NARS2, also known as NAC2 and NAM, respectively) caused aberrant seed shapes in Arabidopsis thaliana. Double knockout mutant nars1 nars2 exhibited abnormally shaped seeds moreover, neither nars1 nor nars2 produced abnormal seeds, indicating that NARS1 and NARS2 redundantly regulate seed morphogenesis. Degeneration of the integuments in nars1 nars2 was markedly delayed, while that of the wild type occurred around the torpedo-shaped embryo stage. Additionally, nars1 nars2 showed a defect in embryogenesis: some nars1 nars2 embryos were developmentally arrested at the torpedo-shaped embryo stage. Unexpectedly, however, neither NARS1 nor NARS2 was expressed in the embryo at this stage, although they were found to be expressed in the outer integument. Wild-type pistils pollinated with nars1 nars2 pollen generated normal seeds, while the reverse crossing generated abnormal seeds. Taken together, these results indicate that NARS1 and NARS2 regulate embryogenesis by regulating the development and degeneration of ovule integuments. Our findings suggest that there is an intertissue communication between the embryo and the maternal integument.
Publisher: Oxford University Press (OUP)
Date: 17-04-2012
DOI: 10.1093/PCP/PCS057
No related grants have been discovered for Mitsuhiro Aida.