Lost genome segments associate with trait diversity during rice domestication.

BACKGROUND: DNA mutations of diverse types provide the raw material required for phenotypic variation and evolution. In the case of crop species, previous research aimed to elucidate the changing patterns of repetitive sequences, single-nucleotide polymorphisms (SNPs), and small InDels during domestication to explain morphological evolution and adaptation to different environments. Additionally, structural variations (SVs) encompassing larger stretches of DNA are more likely to alter gene expression levels leading to phenotypic variation affecting plant phenotypes and stress resistance. Previous studies on SVs in rice were hampered by reliance on short-read sequencing limiting the quantity and quality of SV identification, while SV data are currently only available for cultivated rice, with wild rice largely uncharacterized. Here, we generated two genome assemblies for O. rufipogon using long-read sequencing and provide insights on the evolutionary pattern and effect of SVs on morphological traits during rice domestication. RESULTS: In this study, we identified 318,589 SVs in cultivated and wild rice populations through a comprehensive analysis of 13 high-quality rice genomes and found that wild rice genomes contain 49% of unique SVs and an average of 1.76% of genes were lost during rice domestication. These SVs were further genotyped for 649 rice accessions, their evolutionary pattern during rice domestication and potential association with the diversity of important agronomic traits were examined. Genome-wide association studies between these SVs and nine agronomic traits identified 413 candidate causal variants, which together affect 361 genes. An 824-bp deletion in japonica rice, which encodes a serine carboxypeptidase family protein, is shown to be associated with grain length. CONCLUSIONS: We provide relatively accurate and complete SV datasets for cultivated and wild rice accessions, especially in TE-rich regions, by comparing long-read sequencing data for 13 representative varieties. The integrated rice SV map and the identified candidate genes and variants represent valuable resources for future genomic research and breeding in rice.

Analysis of a rice blast resistance gene Pita-Fuhui2663 and development of selection marker.

Rice blast is a detrimental rice disease caused by the fungus Magnaporthe oryzae. Here, we identified a resistance gene from the rice cultivar Fuhui 2663 which is resistant to the rice blast isolate KJ201. Through isolated population analyses and sequencing approaches, the candidate gene was traced to chromosome 12. With the use of a map-based cloning strategy, the resistance gene was ultimately mapped to an 80-kb resistance locus region containing the Pita gene. Candidate gene prediction and cDNA sequencing indicated that the target resistance gene in Fuhui 2663 was allelic to Pita, thus being referred to as Pita-Fuhui2663 hereafter. Further analysis showed that the Fuhui 2663 protein had one amino acid change: Ala (A) residue 918 in Pita-Fuhui2663 was replaced by Ser (S) in Pita-S, leading to a significant change in the 3D structure of the Pita-S protein. CRISPR/Cas9 knockout experiments confirmed that Pita-Fuhui2663 is responsible for the resistance phenotype of Fuhui 2663. Importantly, Pita-Fuhui2663 did not affect the main agronomic traits of the variety compared to the Pita gene as verified by knockout experiments, indicative of potential applications of Pita-Fuhui2663 in broader breeding programs. Furthermore, a Pita-Fuhui2663-dCAPS molecular marker with good specificity and high efficiency was developed to facilitate rice breeding for resistance to this devastating disease.

The soybean plasma membrane-localized cation/H+ exchanger GmCHX20a plays a negative role under salt stress.

Cation/H+ -exchanger (CHX) perform diverse functions in plants, including being a part of the protective mechanisms to cope with salt stress. GmCHX1 has been previously identified as the causal gene in a major salt-tolerance quantitative trait locus (QTL) in soybean, but little is known about another close paralog, GmCHX20a, found in the same QTL. In this study, GmCHX20a was characterized along with GmCHX1. The expression patterns of the two genes and the direction of Na+ flux directed by overexpression of these two transporters are different, suggesting that they are functionally distinct. The ectopic expression of GmCHX20a led to an increase in salt sensitivity and osmotic tolerance, which was consistent with its role in increasing Na+ uptake into the root. Although this seems counter-intuitive, it may in fact be part of the mechanism by which soybean could counter act the effects of osmotic stress, which is commonly manifested in the initial stage of salinity stress. On the other hand, GmCHX1 from salt-tolerant soybean was shown to protect plants via Na+ exclusion under salt stress. Taken together these results suggest that GmCHX20a and GmCHX1 might work complementally through a concerted effort to address both osmotic stress and ionic stress as a result of elevated salinity.

The Function of Inositol Phosphatases in Plant Tolerance to Abiotic Stress.

Inositol signaling is believed to play a crucial role in various aspects of plant growth and adaptation. As an important component in biosynthesis and degradation of myo-inositol and its derivatives, inositol phosphatases could hydrolyze the phosphate of the inositol ring, thus affecting inositol signaling. Until now, more than 30 members of inositol phosphatases have been identified in plants, which are classified intofive families, including inositol polyphosphate 5-phosphatases (5PTases), suppressor of actin (SAC) phosphatases, SAL1 phosphatases, inositol monophosphatase (IMP), and phosphatase and tensin homologue deleted on chromosome 10 (PTEN)-related phosphatases. The current knowledge was revised here in relation to their substrates and function in response to abiotic stress. The potential mechanisms were also concluded with the focus on their activities of inositol phosphatases. The general working model might be that inositol phosphatases would degrade the Ins(1,4,5)P3 or phosphoinositides, subsequently resulting in altering Ca2+ release, abscisic acid (ABA) signaling, vesicle trafficking or other cellular processes.