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자료유형
학술저널
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한국식물생명공학회 Journal of Plant Biotechnology Journal of Plant Biotechnology 제41권 제4호
발행연도
2014.1
수록면
180 - 193 (14page)

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In plants, a shoot apex has a small region knownas the shoot apical meristem (SAM) having a group of dividing(initiating) cells. The SAM gives rise to all the groundabovestructures of plants throughout their lifetime, and thus itplays important role in growth and development of plants. This review describes theories to explain the SAM organizationand function developed over the last 250 years. Since in 1759German botanist C. F. Wolff has described firstly the SAM,in 1858 Swiss botanist C. Nägeli proposed the apical celltheory from the observation of a large single apical cell in theSAM of seedless vascular plants: however, this view wasrecognized to be unsuitable to seed plants. In 1868, Germanbotanist J. Hanstein suggested the histogen theory: this conceptsubdividing the SAM into dermatogen, periblem, and pleromewas unable to generally apply to seed plants. In 1924, Germanbotanist A. Schmidt proposed the tunica-corpus theory fromthe examination of angiosperm SAM in which two partsshow different planes of cell division: this theory was provedto be not suitable to gymnosperm SAM, not have stablesurface tunica layer. In 1938, American botanist A. Fosterdescribed zones in gymnosperm SAM based on the cytohistologicdifferentiation and thus called it a cytohistological zonationtheory. With works by E. Gifford, in 1954, this zonation patternwas demonstrated to be also applicable to angiosperm SAM. As another theory, in 1952 French botanist R. Buvat proposedthe méristème d’attente (waiting meristem) theory: however,this concept was confuted because of its negation of functionduring vegetative growth phase to central initial cells. Rescentstudies with Arabidopsis thaliana have found that formationand maintenance of the SAM are under the control of selectedgenes: SHOOTMERISTEMLESS (STM) gene forms the SAM,and WUSCHEL (WUS) and CLAVATA (CLV) genes functionin maintaining the SAM; signaling between WUS and CLVgenes act through a negative feedback loop.

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