Somatic and Reproductive Cell Development in Rice Anther Is Regulated by a Putative Glutaredoxin

Somatic and Reproductive Cell Development in Rice Anther Is Regulated by a Putative Glutaredoxin
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DOI:
10.1105/tpc.111.093740
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发表时间:
2012-02-01
期刊:
影响因子:
11.6
通讯作者:
Cheng, Zhukuan
Cheng, Zhukuan
中科院分区:
生物学1区
文献类型:
--
作者:
Hong, Lilan;Tang, Ding;Cheng, Zhukuan

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有丝分裂向减数分裂的转变是真核生物有性生殖过程中最关键的事件之一。然而,协调减数分裂起始的机制仍然难以捉摸,特别是在植物中。有花植物为异孢型,雌雄孢子的发生具有不同的发育过程。在这里,我们表明,植物花粉母细胞包含一个特定的减数分裂起始机制,通过表征水稻(水稻)基因,小孢子囊1(MIL1)。突变体mil1在花药中不产生小孢子,但具有正常的雌性育性。详细的分子和细胞学研究表明,mil1花药在造孢细胞后代的减数分裂进入和周围体细胞层的分化中存在缺陷,导致充满体细胞而不是小孢子的小室。此外,对mil1 msp1双突变体的分析表明,由于缺乏MIL1,其花药室中心的细胞也不激活减数分裂细胞周期,产生与mil1相似的花药表型。MIL1基因编码一种植物特异性的CC型谷氧还蛋白,可与TGA转录因子相互作用。这些结果表明,减数分裂进入小孢子母细胞是由花药特异性机制,这需要MIL1活性,氧化还原调节可能在这个过程中发挥重要作用。
The switch from mitosis to meiosis is one of the most pivotal events in eukaryotes undergoing sexual reproduction. However, the mechanisms orchestrating meiosis initiation remain elusive, particularly in plants. Flowering plants are heterosporous, with male and female spore genesis adopting different developmental courses. We show here that plant pollen mother cells contain a specific meiosis initiation machinery through characterization of a rice (Oryza sativa) gene, MICROSPORELESS1 (MIL1). The mil1 mutant does not produce microspores in anthers but has the normal female fertility. Detailed molecular and cytological investigations demonstrate that mil1 anthers are defective in the meiotic entry of sporogenous cell progenies and in the differentiation of surrounding somatic cell layers, resulting in locules filled with somatic cells instead of microspores. Furthermore, analysis of mil1 msp1 double mutants reveals that due to the absence of MIL1, the cells in their anther locule center do not activate meiotic cell cycle either, generating a similar anther phenotype to mil1. MIL1 encodes a plant-specific CC-type glutaredoxin, which could interact with TGA transcription factors. These results suggest meiotic entry in microsporocytes is directed by an anther-specific mechanism, which requires MIL1 activity, and redox regulation might play important roles in this process.