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水稻 pds1 位点与伙伴基因发生遗传互作,导致穗伸出缺陷和小穗中异位分蘖。

The rice pds1 locus genetically interacts with partner to cause panicle exsertion defects and ectopic tillers in spikelets.

机构信息

College of Life Science and technology (State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources), Guangxi University, Nanning, 530004, China.

Agriculture College, Guangxi University, Nanning, 530004, China.

出版信息

BMC Plant Biol. 2019 May 15;19(1):200. doi: 10.1186/s12870-019-1805-z.

DOI:10.1186/s12870-019-1805-z
PMID:31092192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6521401/
Abstract

BACKGROUND

Rice (Oryza sativa L.) is a staple food crop worldwide. Its yield and quality are affected by its tillering pattern and spikelet development. Although many genes involved in the vegetative and reproductive development of rice have been characterized in previous studies, the genetic mechanisms that control axillary tillering, spikelet development, and panicle exsertion remain incompletely understood.

RESULTS

Here, we characterized a novel rice recombinant inbred line (RIL), panicle exsertion defect and aberrant spikelet (pds). It was derived from a cross between two indica varieties, S142 and 430. Intriguingly, no abnormal phenotypes were observed in the parents of pds. This RIL exhibited sheathed panicles at heading stage. Still, a small number of tillers in pds plants were fully exserted from the flag leaves. Elongated sterile lemmas and rudimentary glumes (occurred occasionally) were observed in the spikelets of the exserted panicles and were transformed into palea/lemma-like structures. Furthermore, more interestingly, tillers occasionally grew from the axils of the elongated rudimentary glumes. Via genetic linkage analysis, we found that the abnormal phenotype of pds manifesting as genetic incompatibility or hybrid weakness was caused by genetic interaction between a recessive locus, pds1, which was derived from S142 and mapped to chromosome 8, and a locus pds2, which not yet mapped from 430. We fine-mapped pds1 to an approximately 55-kb interval delimited by the markers pds-4 and 8 M3.51. Six RGAP-annotated ORFs were included in this genomic region. qPCR analysis revealed that Loc_Os080595 might be the target of pds1 locus, and G1 gene might be involved in the genetic mechanism underlying the pds phenotype.

CONCLUSIONS

In this study, histological and genetic analyses revealed that the pyramided pds loci resulted in genetic incompatibility or hybrid weakness in rice might be caused by a genetic interaction between pds loci derived from different rice varieties. Further isolation of pds1 and its interactor pds2, would provide new insight into the molecular regulation of grass inflorescence development and exsertion, and the evolution history of the extant rice.

摘要

背景

水稻(Oryza sativa L.)是世界范围内的主食作物。其产量和品质受其分蘖模式和小穗发育的影响。尽管之前的研究已经对参与水稻营养和生殖发育的许多基因进行了特征描述,但控制腋芽分蘖、小穗发育和穗抽出的遗传机制仍不完全清楚。

结果

在这里,我们对一种新型水稻重组自交系(RIL),穗抽出缺陷和小穗异常(pds)进行了表征。它是由两个籼稻品种 S142 和 430 杂交而成。有趣的是,pds 的亲本中没有观察到异常表型。该 RIL 在抽穗期表现出包着叶鞘的穗。然而,在 pds 植株中,仍有少量分蘖完全从旗叶中抽出。在抽出的穗中,观察到伸长的不育外稃和发育不全的内稃(偶尔发生),并转化为假稃/外稃样结构。此外,更有趣的是,分蘖偶尔从伸长的发育不全内稃的腋芽中生长。通过遗传连锁分析,我们发现 pds 的异常表型表现为遗传不亲和或杂种弱势,是由一个隐性位点 pds1 和一个尚未从 430 定位的位点 pds2 之间的遗传相互作用引起的。我们将 pds1 精细定位到一个约 55-kb 的区间,该区间由标记 pds-4 和 8M3.51 限定。该基因组区域包含六个 RGAP 注释的 ORF。qPCR 分析显示,Loc_Os080595 可能是 pds1 位点的靶标,而 G1 基因可能参与了 pds 表型的遗传机制。

结论

在这项研究中,组织学和遗传分析表明,来自不同水稻品种的 pds 位点的基因互作可能导致水稻中基因不亲和或杂种弱势的累积 pds 位点,这可能是由不同水稻品种衍生的 pds 位点之间的遗传相互作用引起的。进一步分离 pds1 和其互作 pds2,将为禾本科植物花序发育和抽出的分子调控以及现存水稻的进化历史提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/954d70313b5f/12870_2019_1805_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/2a5203da3a78/12870_2019_1805_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/3fcbbecd354c/12870_2019_1805_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/ee3d1e88aeec/12870_2019_1805_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/ab869b34684e/12870_2019_1805_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/5c8de8d09a01/12870_2019_1805_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/5d4599219c69/12870_2019_1805_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/c9a62377c3f1/12870_2019_1805_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/7f414f292879/12870_2019_1805_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/954d70313b5f/12870_2019_1805_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/2a5203da3a78/12870_2019_1805_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/3fcbbecd354c/12870_2019_1805_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/ee3d1e88aeec/12870_2019_1805_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/ab869b34684e/12870_2019_1805_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/5c8de8d09a01/12870_2019_1805_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/5d4599219c69/12870_2019_1805_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/c9a62377c3f1/12870_2019_1805_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/7f414f292879/12870_2019_1805_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3434/6521401/954d70313b5f/12870_2019_1805_Fig9_HTML.jpg

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