Non-cell-autonomous rescue of anaphase-promoting complex function revealed by mosaic analysis of HOBBIT, an Arabidopsis CDC27 homolog
Non-cell-autonomous rescue of anaphase-promoting complex function revealed by mosaic analysis of HOBBIT, an Arabidopsis CDC27 homolog
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DOI：
10.1073/pnas.0602410103
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发表时间：
2006-08-29
影响因子：
11.1
通讯作者：
Scheres, Ben
中科院分区：
文献类型：
--
作者：
Serralbo, Olivier;Perez-Perez, Jose Manuel;Scheres, Ben
拟南芥HOBBIT（HBT）基因编码的同源物的CDC 27后期促进复合物/环体亚基，是胚胎后发育所必需的。我们通过Cre/lox介导的单个互补HBT转基因在强突变等位基因hbt（2311）纯合的背景中重组来诱导功能丧失克隆。细胞分裂和细胞扩增的缺陷是普遍存在的胚后HBT切除的主要后果。在根中，细胞分裂和细胞扩张都迅速受到影响。相反，在叶原基中，细胞分裂和细胞扩张在滞后期后停止，这导致proximodistal和mediolateral轴中不同程度的缺陷。令人惊讶的是，小克隆揭示了hbt突变细胞的非细胞自主拯救，表明了一种以前未被认识到的对细胞周期进展至关重要的后期促进复合物/细胞周期小体组分活性降低的补偿机制。
The Arabidopsis HOBBIT (HBT) gene encodes a homolog of the CDC27 anaphase-promoting complex/cyclosome subunit and is essential for postembryonic development. We induced loss-of-function clones by Cre/lox-mediated recombination of a single complementing HBTtransgene in a background homozygous for the strong mutant allele hbt(2311). Defects in cell division and cell expansion are the primary consequences of ubiquitous postembryonic HBT excision. In roots, both cell division and cell expansion are rapidly affected. In contrast, in leaf primordia, cell division and cell expansion halt after a lag phase, which results in different severities of defects in the proximodistal and mediolateral axes. Surprisingly, small clones reveal non-cell-autonomous rescue of hbt mutant cells, indicating a previously unrecognized compensation mechanism for reduced activity of an anaphase-promoting complex/cyclosome component critical for cell cycle progression.