|PubMed ID||26925070 Pubmed||日付||2016//|
|タイトル||Suppressor Screen and Phenotype Analyses Revealed an Emerging Role of the Monofunctional Peroxisomal Enoyl-CoA Hydratase 2 in Compensated Cell Enlargement.|
|ジャーナル||Frontiers in plant science 2016// 7() 132|
|著者||Katano Mana M,Takahashi Kazuki K,Hirano Tomonari T,Kazama Yusuke Y,Abe Tomoko T,Tsukaya Hirokazu H,Ferjani Ali A|
|抄録||Efficient use of seed nutrient reserves is crucial for germination and establishment of plant seedlings. Mobilizing seed oil reserves in Arabidopsis involves β-oxidation, the glyoxylate cycle, and gluconeogenesis, which provide essential energy and the carbon skeletons needed to sustain seedling growth until photoautotrophy is acquired. We demonstrated that H(+)-PPase activity is required for gluconeogenesis. Lack of H(+)-PPase in fugu5 mutants increases cytosolic pyrophosphate (PPi) levels, which partially reduces sucrose synthesis de novo and inhibits cell division. In contrast, post-mitotic cell expansion in cotyledons was unusually enhanced, a phenotype called compensation. Therefore, it appears that PPi inhibits several cellular functions, including cell cycling, to trigger compensated cell enlargement (CCE). Here, we mutagenized fugu5-1 seeds with (12)C(6+) heavy-ion irradiation and screened mutations that restrain CCE to gain insight into the genetic pathway(s) involved in CCE. We isolated A#3-1, in which cell size was severely reduced, but cell number remained similar to that of original fugu5-1. Moreover, cell number decreased in A#3-1 single mutant (A#3-1sm), similar to that of fugu5-1, but cell size was almost equal to that of the wild type. Surprisingly, A#3-1 mutation did not affect CCE in other compensation exhibiting mutant backgrounds, such as an3-4 and fugu2-1/fas1-6. Subsequent map-based cloning combined with genome sequencing and HRM curve analysis identified enoyl-CoA hydratase 2 (ECH2) as the causal gene of A#3-1. The above phenotypes were consistently observed in the ech2-1 allele and supplying sucrose restored the morphological and cellular phenotypes in fugu5-1, ech2-1, A#3-1sm, fugu5-1 ech2-1, and A#3-1; fugu5-1. Taken together, these results suggest that defects in either H(+)-PPase or ECH2 compromise cell proliferation due to defects in mobilizing seed storage lipids. In contrast, ECH2 alone likely promotes CCE during the post-mitotic cell expansion stage of cotyledon development, probably by converting indolebutyric acid to indole acetic acid.|
Putative role of Auxin in CCE
東京学芸大学自然科学系生命科学分野 Ferjani Ali研究室 Ferjani Ali 投稿日時[2016-03-02 19:25:03]
In the present study, we mutagenized fugu5-1 seeds with heavy-ion irradiation, and screened for mutations that either partially or totally restrain CCE. Importantly, we found that a mutation in the Peroxisomal Enoyl-CoA Hydratase 2 (ECH2) totally suppressed CCE in fugu5. Interestingly, as shown in this study, the ech2-1 mutation did not affect at all CCE in other compensation-exhibiting mutants, such as fasciata1-6 and angustifolia3-4. Based on our results, we suggest a working model for regulation of CCE in fugu5, where the dual functions of ECH2 (TAG mobilization and IBA-to-IAA conversion) likely play a key role in CCE in fugu5 background.
In brief, the major outcome of this study is that "AUXIN" might be a candidate molecule to answer some of our longstanding questions about CCE in fugu5.
** Abbreviations: TAG: triacylglycerol; IBA: indolebutyric acid; IAA: indole acetic acid.
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