MAPK是调节植物个体大小的开关
It's long been debated how similar plant and animal development are. So the identification of a mitogen-activated protein kinase kinase (MAPKK) kinase gene that promotes extra-embryonic cell fate in Arabidopsis thaliana, reported in Cell by Lukowitz and colleagues, might add to this similarity.
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In A. thaliana embryogenesis, the zygote divides asymmetrically into a small cell that sits on top of a larger cell. These two cells then establish fundamentally different lineages — the apical lineage develops into the proembryo, and the basal lineage develops into a largely extra-embryonic structure, the 'suspensor'. To understand what mediates this segregation of fates, the authors carried out a search for mutations that affect early embryo development. Mutations in YODA (YDA) resulted in the formation of embryos that lacked a well-formed suspensor. Whereas wild-type zygotes elongate before dividing, yda embryos were, at an equivalent stage, only about half the length; the apical cells were the same size as the wild-types, but the basal cells were much smaller. The basal cells usually divide transversely into a file of highly vacuolated cells, but mutant basal cells often divide longitudinally instead, and lack a prominent vacuole. So loss-of-function of YDA seems to inhibit suspensor development.
Coincident with this, yda embryos also showed no signs of forming roots or establishing a body axis early in embryogenesis. However, a fraction of them were eventually able to give rise to complete seedlings and developed into dwarfed and sterile plants. Because of this dwarfism, the authors supposed that YDA might function in a general hormone-signal-transduction pathway. However, they were unable to place YDA in any known hormone or signalling pathway, which indicates that YDA might be part of a new developmental signalling pathway.
Lukowitz and colleagues found that YDA corresponds to a gene encoding a protein that strongly resembles a MAPKK kinase. The yda mutations are expected to negatively affect kinase activity. The authors also created deletions on the amino-terminal side of the catalytic domain of YDA, as this region is often involved in repressing catalytic activity. These alleles complemented the mutant phenotype, but also gave rise to new gain-of-function phenotypes. Embryos that had amino-terminal deletions of YDA generally developed slightly larger basal cells and larger suspensors. In the most extreme cases, development of the proembryo was completely inhibited.
So the authors propose that YDA acts as part of a cell-fate switch that promotes extra-embryonic fate. The next challenge is to identify the upstream and downstream components of this signalling pathway.
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References and links
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ORIGINAL RESEARCH PAPER Nature Reviews Molecular Cell Biology 5, 82-83 (2004); doi:10.1038/nrm1325 [PDF file 665K] |
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