著者
Mizuki Yamada Shunsuke Tanaka Tatsuya Miyazaki Mitsuhiro Aida
出版者
Japanese Society for Plant Biotechnology
雑誌
Plant Biotechnology (ISSN:13424580)
巻号頁・発行日
vol.39, no.1, pp.37-42, 2022-03-25 (Released:2022-03-25)
参考文献数
32
被引用文献数
4

During embryogenesis of eudicots, the apical region of the embryo develops two cotyledon primordia and the shoot meristem. In Arabidopsis thaliana, this process is dependent on the functionally redundant activities of the CUP-SHAPED COTYLEDON (CUC) transcription factors, namely CUC1, CUC2, and CUC3, as well as the phytohormone auxin. However, the relationship between the CUC proteins and auxin has yet to be fully elucidated. In the present study, we examined whether the expression of auxin biosynthetic genes is dependent on CUC gene activities. Comprehensive quantitative RT-PCR analysis of the main auxin biosynthetic gene families of TRYPTOPHAN AMINOTRANSFERASE OF ARABIDOPSIS1/TRYPTOPHAN AMINOTRANSFERASE RELATED and YUCCA (YUC) showed that YUC1 and YUC4 expression levels were lower in cuc double mutant embryos than the expression levels of these genes in wild type embryos. Reporter analysis also revealed that the expression of YUC1 and YUC4 in the cotyledon boundary region was reduced in cuc double mutant embryos. In contrast, the loss of function mutation in the SHOOT MERISTEMLESS gene, a shoot stem cell regulator that acts downstream of the CUC genes, did not markedly affect YUC1 expression levels. These results demonstrate that CUC genes play an important role in the regulation of auxin biosynthetic gene expression during embryogenesis; furthermore, they raise the possibility that the auxin produced by this regulation contributes to cotyledon boundary development.
著者
Hiroki Ueno Takeshi Maeda Naoki Katsuyama Yu Katou Satoshi Matsuo Kanako Yano Akira Ando Kaori Nagasuga Mizuki Yamada Shunsuke Imanishi
出版者
一般社団法人 園芸学会
雑誌
The Horticulture Journal (ISSN:21890102)
巻号頁・発行日
pp.OKD-101, (Released:2017-10-11)
被引用文献数
11

Several Japanese tomato cultivars develop a physiological disorder called leaf marginal necrosis, which occurs in relatively young compound leaves. Although the positions of the observed symptoms differ from those caused by inadequate potassium (K+) supplementation, previous studies have reported a relationship between the reduction of K+ content and the occurrence of this disorder. However, the mechanism of the relationship between K+ deficiency and leaf marginal necrosis remains unstudied. In the present study, the relationship between K+ deficiency in leaflets and leaf marginal necrosis was investigated by cation measurement and gene expression analysis to understand the possible mechanism responsible for the induction of leaf marginal necrosis. First, cation measurement of the two cultivars differing in their symptom intensities showed a trend of K+ reduction in the ‘CF Momotaro J’ cultivar developing leaf marginal necrosis at the tip leaflets positioned under the flowering fruit truss. Next, a comparison between the basal and tip region of the leaflet from four cultivars differing in their symptom intensities revealed that the K+ concentration in tip leaflets was significantly lower in the tip regions compared to the basal region, especially in the two cultivars ‘CF Momotaro J’ and ‘Momotaro grande’, leading to leaf marginal necrosis. The gene expression analysis of the basal and tip regions identified that the expression patterns of jasmonate-related genes were upregulated in the tomato leaflets with low K+ concentration. The gene expression of a leaf senescence marker gene, a homologue of the SAG12 gene of Arabidopsis thaliana, was detected only in the leaf tip region samples with the lowest K+ concentration. Furthermore, ‘CF Momotaro J’ plants cultivated with K+-supplemented medium showed an increase in the K+ concentration, a decrease in the occurrence of leaf marginal necrosis, and down-regulation of the expression of jasmonate-related genes in tip leaflets. These results indicate that tomato leaf marginal necrosis occurs because of K+ starvation in the tip region of leaflets, leading to the activation of jasmonate-induced signal for necrosis.