DNA marker-assisted selection (MAS) has become an indispensable component of breeding. Single nucleotide polymorphisms (SNP) are the most frequent polymorphism in the rice genome. However, SNP markers are not readily employed in MAS because of limitations in genotyping platforms. Here the authors report a Golden Gate SNP array that targets specific genes controlling yield-related traits and biotic stress resistance in rice. As a first step, the SNP genotypes were surveyed in 31 parental varieties using the Affymetrix Rice 44K SNP microarray. The haplotype information for 16 target genes was then converted to the Golden Gate platform with 143-plex markers. Haplotypes for the 14 useful allele are unique and can discriminate among all other varieties. The genotyping consistency between the Affymetrix microarray and the Golden Gate array was 92.8%, and the accuracy of the Golden Gate array was confirmed in 3 F2 segregating populations. The concept of the haplotype-based selection by using the constructed SNP array was proofed.
Gibberellin (GA) is one of the plant hormones which regulates many aspects of plant growth and developmental processes. Rice plants known as deepwater rice can survive during flooding by elongating its internodes to avoid anoxia. Previous studies reported that GA is essential for internode elongation in deepwater rice. However, the interaction between internode elongation and regulator of GA sensitivity is unknown. In this study, we performed a QTL analysis and identified the chromosomal regions that regulate GA responsiveness in deepwater rice. We concluded that deepwater rice could induce internode elongation in response to GA by factors in these regions.
BackgroundGrain size is an important trait that affects rice yield. Although many genes that contribute to grain size have been cloned from mutants or by quantitative trait locus (QTL) analysis based on bi-parental mapping, the molecular mechanisms underlying grain-size determination remain poorly understood. In this study, we identified the lines with the largest grain size and detected novel QTLs affecting the grain size.ResultsWe screened the National Institute for Agrobiological Sciences Genebank database and identified two rice lines, BG23 with the widest grain and LG10 with the longest grain. Using these two lines, we performed QTL analysis for grain size. Eight QTLs were detected during the QTL analyses using F2 populations derived from crosses between the large-grain lines BG23 or LG10 and the middle-size grain cultivars Nipponbare and Kasalath. Both BG23 and LG10 possessed large-grain alleles of four major QTLs: GW2, GS3, qSW5/GW5, and GW8. Other three minor QTLs were derived from BG23. However, these QTLs did not explain the differences in grain size between these two lines. Additionally, four QTLs for grain length or width were detected in an F2 population derived from a cross between BG23 and LG10; this population lacked the strong effects of the four major QTLs shared by both parent plants. Of these newly detected QTLs, the effects of two QTLs, GL3b and GL6, were confirmed by progeny testing. Comparison of the length of inner epidermal cells in plants homozygous for BG23 and LG10 alleles indicated that GL3b and GL6 genes regulate cell elongation and cell division, respectively.ConclusionsIn this study, we detected 12 loci including 14 QTLs regulating grain size from two lines with largest grains available in Japanese stock. Of these loci, we confirmed the effect of two gene loci and mapped their candidate region. Identification of novel genes regulating grain size will contribute to our understanding of the molecular mechanisms controlling grain size.Electronic supplementary materialThe online version of this article (doi:10.1186/s12284-016-0109-2) contains supplementary material, which is available to authorized users.
The endoplasmic reticulum (ER) is an essential organelle required for the folding and maturation of newly synthesized secretory and transmembrane proteins. Several biochemical and physiological conditions interfere with the correct folding of proteins, leading to the accumulation of unfolded or misfolded proteins in the ER. These conditions are called ER stress and elicit stress response signaling, collectively termed the unfolded protein response (UPR). 6 The UPR is regulated by 3 stress sensor proteins located at the ER membrane; inositol-requiring protein 1α (IRE1α), protein kinase regulated by RNA-like ER kinase, and activating transcription factor 6. The UPR signaling reduces the protein load that enters the ER and increases the protein folding capacity, attempting to reestablish and maintain the homeostasis of the ER. 7 However, when homeostasis cannot be re-established, the UPR leads to cell apoptosis. ER stress has been considered to play a key role in the pathogenesis of several diseases, such as neurological diseases, diabetes mellitus, and atherosclerosis. Objective-The accumulation of unfolded protein in the endoplasmic reticulum (ER) initiates an adaptive stress response, termed the unfolded protein response. Previous studies suggested that ER stress might be involved in the formation of neointima after vascular injury. We recently discovered a novel regulator of ER stress, 78-kDa glucose-regulated protein-interacting protein induced by ER stress (Gipie). The objective of this study was to elucidate the role of Gipie using models of vascular disease. Approach and Results-We investigated the functions of Gipie in cultured vascular smooth muscle cells (VSMCs) and in a vascular injury model of a rat carotid artery. The expression of Gipie was predominantly detected in synthetic VSMCs and to a much lesser extent in contractile VSMCs, which was augmented by treatment with thapsigargin. Gipie knockdown increased the phosphorylation levels of c-Jun N-terminal kinase and the number of apoptotic cells under ER stress. Moreover, Gipie knockdown decreased the mature form of collagen I in synthetic VSMCs. The expression of Gipie was rarely detected in the medial VSMCs of the intact carotid artery, whereas it was detected in most of the neointimal cells and some of the medial VSMCs after balloon injury. Depletion of Gipie in the rat carotid artery attenuated the neointimal thickening, which was accompanied by increased cell death in the neointima. Conversely, overexpression of Gipie augmented the neointimal thickening. Conclusions-Gipie
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