首页> 外文期刊>Acta Horticulturae >Characterizing cell divisions and cell identity in Atdek1 mutant embryos by cytoskeletal studies and localization of the AtML1 , WUS and STM meristem markers.
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Characterizing cell divisions and cell identity in Atdek1 mutant embryos by cytoskeletal studies and localization of the AtML1 , WUS and STM meristem markers.

机译:通过细胞骨架研究和 AtML1 , WUS 和 STM 的细胞骨架研究来表征 Atdek1 突变体胚胎中的细胞分裂和细胞身份分生组织标记。

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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 Atdek1 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 Atdek1 embryogenesis was monitored by in situ hybridization with the molecular markers WUS, STM, AtML1 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 Atdek1 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 Atdek1 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:在胚胎发生过程中,细胞分裂平面受到严格控制,这说明了分裂平面正确定位和定向的重要性。 L1和L2层进一步保留了它们的克隆身份,并表现出抗胶质细胞分裂,而内部细胞表现出了近缘细胞分裂。在胚胎发生过程中,不同的细胞会根据原始细胞谱系和位置同一性假定不同的细胞命运,这也对应于特定的基因表达谱。 DEFECTIVE KERNEL1 ( DEK1 )是表皮细胞形成的位置依赖性分化的关键基因。 DEK1具有几个特性,这些特性与表皮细胞命运中的细胞间通信角色以及L1,规格和维护兼容。我们在这里提出了分别在野生型和 Atdek1 胚胎中的有丝分裂机制,即微管蛋白和肌动蛋白的研究。出乎意料的是,基于对dek1胚胎表型的观察,观察到有丝分裂周期的所有阶段以及前期带和早期成膜细胞。然而,经常观察到由于随机细胞壁沉积而导致的切口和消融细胞以及不相等的细胞大小。通过分子标记 WUS , STM , AtML1的原位杂交,监测 Atdek1 胚胎发生过程中不同区域的组织和细胞身份和 WOX8 。发现 WUS 和 STM 相对于野生型在空间上发生了变化,它们被扩大并且明显地具有较小的区域特异性。 AtML1 似乎在 Atdek1 胚胎中表现出斑片状的L1层,而 WOX8 显示了根尖基极的存在。综上所述,这些结果使我们认为 Atdek1 表型的潜在主要机制与无组织的分裂方向和细胞壁沉积有关,缺乏限制而不是缺乏细胞类型的规范。

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