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Characterizing Cell Divisions and Cell Identity in Atdek1 Mutant Embryos by Cytoskeletal Studies and Localization of the AtMLI, WUS and STM Meristem Markers

机译:通过细胞骨骼研究和ATMLI,WU​​S和STM公司标记的细胞骨骼研究和定位在ATDEK1突变体胚胎中的细胞分裂和细胞同一性

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During embryogenesis cell division planes are tightly controlled illustrating the importance of correct positioning and orientation of division planes. The L1 and L2 layers further keep their clonal identity and exhibit anticlinal division while the inner cells exhibit periclinal divisions. During embryogenesis different cells assume different cell fates from original cell lineage and positional identity, which also correspond to specific gene expression profiles. DEFECTIVE KERNEL1 (DEK1) is a crucial gene for position dependent differentiation of epidermal cell formation. DEK1 possesses several characteristics that are compatible with a role in cell-cell communication in epidermal cell fate, and also L1, specification and maintenance. We here present a study of the mitotic machinery, hence tubulin and actin, in wild type and Atdekl embryos respectively. Surprisingly, based on observations of the dek1 embryo phenotype, all stages of the mitotic cycle as well as preprophase bands and early phragmoplast, were observed. However, notched and ablated cells as well as unequal cells sizes due to random cell wall deposition were frequently observed. The tissue and cell identity of different regions during Atdekl embryogenesis was monitored by in situ hybridization with the molecular markers WUS, STM, AtMLI and WOX8. WUS and STM were found to be spatially altered relatively to wild type, being enlarged and apparently less region specific. AtML1 seems to exhibit patchy L1 layer in Atdekl embryos, and WOX8 showed that the apical-basal polarity was maintained. Taken together, these results lead us to suggest that the principal mechanism underlying the Atdekl phenotypes are associated with unorganized division orientation and cell wall deposition, and lack of restriction rather than lack of specification of cell types.
机译:在胚胎发生期间,细胞分裂平面紧密控制,说明了分割平面的正确定位和取向的重要性。 L1和L2层进一步保持其克隆标识,并且在内部电池表现出垂直分割时表现出抗冲击划分。在胚胎发生期间,不同的细胞呈现来自原始细胞谱系和位置同一性的不同细胞率,其也对应于特定的基因表达谱。缺陷的kernel1(dek1)是表皮细胞形成的位置依赖性分化的关键基因。 DEK1具有几种与表皮细胞命运中细胞 - 细胞通信中的作用相容的特征,以及L1,规格和维护。我们在这里分别介绍了野生型和ATDEKL胚胎中的有丝分裂机械,因此管蛋白和肌动蛋白的研究。令人惊讶的是,基于DEK1胚胎表型的观察,观察到有丝分裂循环的所有阶段以及蛋白质带和早期的脊椎网。然而,经常观察到由于随机细胞壁沉积引起的缺口和烧蚀细胞以及不等细胞尺寸。通过与分子标记杂交的原位杂交来监测不同区域的组织和细胞同一性,用分子标记杂交,STM,ATMLI和WOX8。发现WUS和STM在空间上相对于野生型变化,被扩大并且明显较少的区域。 ATML1似乎在ATDEKL胚胎中表现出斑块L1层,并且WOX8显示了维持了顶端基极性。总之,这些结果导致我们建议,ATDEKL表型底层的主要机制与无组织划分和细胞壁沉积有关,缺乏限制而不是缺乏细胞类型的规格。

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