4.6 Article

Transcriptome analysis of grain-filling caryopses reveals the potential formation mechanism of the rice sugary mutant

期刊

GENE
卷 546, 期 2, 页码 318-326

出版社

ELSEVIER
DOI: 10.1016/j.gene.2014.05.059

关键词

Rice; Transcriptome; Starch-synthesis related genes; sugary mutant; ADP-glucose pyrophosphorylase

资金

  1. National Research Foundation of Korea (NRF) - Korean Ministry of Education, Science and Technology [2010-0022616]
  2. BioGreen 21 Program, Rural Development Administration, Republic of Korea [PJ009099]
  3. National Research Foundation of Korea [2010-0022616] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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A sugary mutant with low total starch and high sugar contents was compared with its wild type Sindongjin for grain-filling caryopses. In the present study, developing seeds of Sindongjin and sugary mutant from the 11th day after flowering (DAF) were subjected to RNA sequencing (RNA-Seq). A total of 30,385 and 32,243 genes were identified in Sindongjin and sugary mutant. Transcriptomic change analysis showed that 7713 differentially expressed genes (DEGs) (log(2) fold change >= 1, false discovery rate (FDR) <= 0.001) were identified based on our RNA-Seq data, with 7239 genes up-regulated and 474 down-regulated in the sugary mutant. A large number of DEGs were found related to metabolic, biosynthesis of secondary metabolites, plant-pathogen interaction, plant hormone signal transduction and starch/sugar metabolism. Detailed pathway dissection and quantitative real time PCR (qRT-PCR) demonstrated that most genes involved in sucrose to starch synthesis are up-regulated, whereas the expression of the ADP-glucose pyrophosphorylase small subunit (OsAGPS2b) catalyzing the first committed step of starch biosynthesis was specifically inhibited during the grain-filling stage in sugary mutant Further analysis suggested that the OsAGPS2b is a considerable candidate gene responsible for phenotype of sugary mutant. (C) 2014 Elsevier B.V. All rights reserved.

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