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Additional file 2: Fig. S11. Syntenic block dotplot within F. esculentum genome. Fig. S12. Syntenic block dotplot between F. esculentum and S. oleracea genomes. Fig. S13. Gene ontology (GO) enrichment analysis of the expanded gene families in F. tataricum. Fig. S14. GO enrichment analysis of the expanded gene families in F. esculentum. Fig. S15. Overview of the rutin biosynthetic pathway in F. tataricum and F. esculentum with expression profiles of key enzyme genes. Fig. S16. Multiple sequence alignment of the UGT2 proteins for the 4 assemblies. Red box indicates the position of UDP-glycosyltransferase functional domian (PF00201). Fig. S17. Sequence alignment of UGT2 promoter sequences in F. tataricum and F. esculentum haplotyped genomes. Fig. S18. Gene collinear relationship between F. tataricum (n=8) and F. esculentum (n=8) genomes. Red lines indicate S-RNase genes loci while blue lines indicate SLF genes loci. Fig. S19 Multiple sequence alignment of the S-RNase proteins for the 2 assemblies. Fig. S20 Sequence alignment of S-RNase promoter sequences in F. tataricum and F. esculentum genomes. Fig. S21. The number of different families within the Copia (a) and Gypsy (b) superfamilies. Fig. S22. The genome comparison between the 2 Mb to 3 Mb interval of Chromosome 8 of Fe-haplotype 1 and FES_r1.0.

Additional file 1: Fig. S1. PacBio long reads (2 cell) length distribution of F. esculentum. Fig. S2. Genome size and heterozygosity estimation for F. esculentum. Fig. S3. Hi-C map of the Fe-haplotype 1 showing genome-wide all-by-all interactions. The map shows a high resolution of individual chromosomes that are scaffolded and assembled independently. Fig. S4. Hi-C map of the Fe-haplotype 2 showing genome-wide all-by-all interactions. The map shows a high resolution of individual chromosomes that are scaffolded and assembled independently. Fig. S5. Genome size and heterozygosity estimation for F. tataricum. Fig. S6. PacBio long reads (1 cell) length distribution of F. tataricum. Fig. S7. Hi-C map of the Ft-haplotype 1 showing genome-wide all-by-all interactions. The map shows a high resolution of individual chromosomes that are scaffolded and assembled independently. Fig. S8. Hi-C map of the Ft-haplotype 2 showing genome-wide all-by-all interactions. The map shows a high resolution of individual chromosomes that are scaffolded and assembled independently. Fig. S9. Genome alignment between F. tataricum cv. Pinku1 and Ft-haplotype 1. Fig. S10. Genome alignment between F. tataricum cv. Pinku1 and Ft-haplotype 2.

Populations of widespread species are usually geographically distributed through contrasting stresses, but underlying genetic mechanisms controlling this adaptation remain largely unknown. Here, we show that in Arabidopsis thaliana, allelic changes in the cis-regulatory elements, WT box and W box, in the promoter of a key transcription factor associated with oxygen sensing, RELATED TO AP 2.12 (RAP2.12), are responsible for differentially regulating tolerance to drought and flooding. These two cis-elements are regulated by different transcription factors that downstream of RAP2.12 results in differential accumulation of hypoxia-responsive transcripts. The evolution from one cis-element haplotype to the other is associated with the colonization of humid environments from arid habitats. This gene thus promotes both drought and flooding adaptation via an adaptive mechanism that diversifies its regulation through noncoding alleles.

Persistent hypotonic and inflammatory conditions in the joint cavity can lead to the loss of cartilage matrix and cell death, which are the important mechanisms of osteoarthritis (OA) onset. Previous studies have confirmed that the existence of a hypotonic environment is a red flag for inflammation, as hypotonic environment induces the opening of the chloride channel of the cell and promotes chloride ion efflux, which prompts the cell volume to increase. Chloride channels play an important role in the regulation of mineralization and chondrocyte death. Here, we reported that OA chondrocytes showed a significant increase of cell death rate and the imbalance of cartilage matrix catabolism. We found that the distribution of skeleton protein F-actin was disordered. In addition, the volume-sensitive chloride current of OA chondrocytes decreased significantly with the increase of the expression levels of inflammation-related proteins caspase-1, caspase-3, and NLRP3. Moreover, interleukin-1β (IL-1β) showed a potential to activate the chloride current of normal chondrocytes. These results indicate that IL-1β-induced chloride channel opening in chondrocytes may be closely related to the occurrence of OA. This chloride channel opening process may therefore be a potential target for the treatment of OA.

Huankun Fang,1,2,* Zhiqin Deng,1,* Jianquan Liu,1,* Siyu Chen,3 Zhenhan Deng,3 Wencui Li1 1Hand and Foot Surgery Department, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen, Guangdong, 518035, People’s Republic of China; 2Medical College, Shantou University, Shantou, Guangdong, 515041, People’s Republic of China; 3Department of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen, Guangdong, 518035, People’s Republic of China*These authors contributed equally to this workCorrespondence: Zhenhan Deng, Department of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, 3002 Sungang West Road, Shenzhen City, 518025, People’s Republic of China, Tel +86 13928440786, Fax +86 755-83366388, Email dengzhenhan@email.szu.edu.cn Wencui Li, Department of Hand and Foot Surgery, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, 3002 Sungang West Road, Shenzhen City, 518025, People’s Republic of China, Tel +86 13923750767, Email wencuilisz@126.comAbstract: Senescence mainly manifests as a series of degenerative changes in the morphological structure and function of the body. Osteoporosis is a systemic bone metabolic disease characterized by destruction of bone microstructure, low bone mineral content, decreased bone strength, and increased brittleness and fracture susceptibility. Osteoblasts, osteoclasts and osteocytes are the main cellular components of bones. However, in the process of aging, due to various self or environmental factors, the body’s function and metabolism are disordered, and osteoporosis will appear in the bones. Here, we summarize the mechanism of aging, and focus on the impact of aging on bone remodeling homeostasis, including the mechanism of ion channels on bone remodeling. Finally, we summarized the current clinical medications, targets and defects for the treatment of osteoporosis.Keywords: aging, osteoporosis, bone formation, epigenetics, autophagy, chlorine channel

Zicong Lin,1,* Zhiqin Deng,1,* Jianquan Liu,1,* Zhongshi Lin,2 Siyu Chen,3 Zhenhan Deng,3 Wencui Li1 1Hand and Foot Surgery Department, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen, Guangdong, 518035, People’s Republic of China; 2Shenzhen Institute for Drug Control (Shenzhen Testing Center of Medical Devices), Shenzhen, Guangdong, 518057, People’s Republic of China; 3Department of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen, Guangdong, 518035, People’s Republic of China*These authors contributed equally to this workCorrespondence: Zhenhan Deng, Department of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, 3002 Sungang West Road, Shenzhen City, 518025, People’s Republic of China, Tel +86 13928440786, Fax +86 755-83366388, Email dengzhenhan@email.szu.edu.cn Wencui Li, Department of Hand and Foot Surgery, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, 3002 Sungang West Road, Shenzhen City, 518025, People’s Republic of China, Tel +86 13923750767, Email liwencui@email.szu.edu.cnAbstract: Articular cartilage allows the human body to buffer and absorb stress during normal exercise. It is mainly composed of cartilage cells and the extracellular matrix and is surrounded by the extracellular microenvironment formed by synovial fluid and various factors in it. Studies have shown that chondrocytes are the metabolic center of articular cartilage. Under physiological conditions, the extracellular matrix is in a dynamic balance of anabolism and catabolism, and various factors and physical and chemical conditions in the extracellular microenvironment are also in a steady state. This homeostasis depends on the normal function of proteins represented by various ion channels on chondrocytes. In mammalian chondrocyte species, ion channels are mainly divided into two categories: cation channels and anion channels. Anion channels such as chloride channels have become hot research topics in recent years. These channels play an extremely important role in various physiological processes. Recently, a growing body of evidence has shown that many pathological processes, abnormal concentration of mechanical stress and chloride channel dysfunction in articular cartilage lead to microenvironment disorders, matrix and bone metabolism imbalances, which cause partial aseptic inflammation. These pathological processes initiate extracellular matrix degradation, abnormal chondrocyte death, hyperplasia of inflammatory synovium and bony. Osteoarthritis (OA) is a common clinical disease in orthopedics. Its typical manifestations are joint inflammation and pain caused by articular cartilage degeneration, but its pathogenesis has not been fully elucidated. Focusing on the physiological functions and pathological changes of chloride channels and pathophysiology of aseptic inflammation furthers the understanding of OA pathogenesis and provides possible targets for subsequent medication development.Keywords: osteoarthritis, chondrocyte, ion channel, inflammatory factors