Genome-Wide Discovery of Microsatellite Markers from Diploid Progenitor Species, Arachis duranensis and A. ipaensis, and Their Application in Cultivated Peanut (A. hypogaea)

Abstract

Despite several efforts in the last decade toward development of simple sequence repeat (SSR) markers in peanut, there is still a need for more markers for conducting different genetic and breeding studies. With the effort of the International Peanut Genome Initiative, the availability of reference genome for both the diploid progenitors of cultivated peanut allowed us to identify 135,529 and 199,957 SSRs from the A (Arachis duranensis) and B genomes (Arachis ipaensis), respectively. Genome sequence analysis showed uneven distribution of the SSR motifs across genomes with variation in parameters such as SSR type, repeat number, and SSR length. Using the flanking sequences of identified SSRs, primers were designed for 51,354 and 60,893 SSRs with densities of 49 and 45 SSRs per Mb in A. duranensis and A. ipaensis, respectively. In silico PCR analysis of these SSR markers showed high transferability between wild and cultivated Arachis species. Two physical maps were developed for the A genome and the B genome using these SSR markers, and two reported disease resistance quantitative trait loci (QTLs), qF2TSWV5 for tomato spotted wilt virus (TSWV) and qF2LS6 for leaf spot (LS), were mapped in the 8.135 Mb region of chromosome A04 of A. duranensis. From this genomic region, 719 novel SSR markers were developed, which provide the possibility for fine mapping of these QTLs. In addition, this region also harbors 652 genes and 49 of these are defense related genes, including two NB-ARC genes, three LRR receptor-like genes and three WRKY transcription factors. These disease resistance related genes could contribute to resistance to viral (such as TSWV) and fungal (such as LS) diseases in peanut. In summary, this study not only provides a large number of molecular markers for potential use in peanut genetic map development and QTL mapping but also for map-based gene cloning and molecular breeding.

Environmental pollutants damage airway epithelial cell cilia: Implications for the prevention of obstructive lung diseases

“…Formaldehyde, acrolein, phenols, and ammonia, which are usually present in indoor air pollutants, have an effect on ciliary oscillations and structure, as well as mucous flow, which may be a cause of respiratory disease. [51][52][53] Formaldehyde has the strongest effect, followed by acrolein. 54,55 After exposure to acrolein, the tip of the cilia is swollen, making the cilia function abnormally; formaldehyde and ammonia reduce the flow of the sputum, which causes functional damage to the MCC.…”

“…Formaldehyde, acrolein, phenols, and ammonia, which are usually present in indoor air pollutants, have an effect on ciliary oscillations and structure, as well as mucous flow, which may be a cause of respiratory disease . Formaldehyde has the strongest effect, followed by acrolein .…”

Therapeutic targeting of cellular stress responses in cancer

“…Binding of RPA is followed by the recruitment of the protein kinase ATR to activate the ATR‐CHK1 axis. Although this process is usually referred to as the replication stress response (RSR), the ATR‐CHK1 axis is also integrated into a more complex signal transduction pathway termed the DNA damage response (DDR), which includes multiple cell cycle checkpoints that dictate the fate of cancer cells depending on whether the damage can be repaired …”

“…Although this process is usually referred to as the replication stress response (RSR), the ATR-CHK1 axis is also integrated into a more complex signal transduction pathway termed the DNA damage response (DDR), which includes multiple cell cycle checkpoints that dictate the fate of cancer cells depending on whether the damage can be repaired. [121][122][123] A number of chemotherapy drugs exert stress on the cancer genome, most of which act as genotoxicants that damage the DNA and induce the DDR; these include DNA cross-linkers, topoisomerase poisons, and alkylating agents. [124][125][126] Although conventional anticancer agents were developed to selectively target highly proliferative cancer cells over normal cells, highly proliferative normal tissues (e.g.…”

CYLD deficiency promotes pancreatic cancer development by causing mitotic defects

“…As previously described (C. Zhao et al, ; Guo et al, ; Han et al, ; H. Li et al, ; Ren et al, ), total RNA was isolated using the PureLink RNA Mini Kit (Thermo Fisher Scientific, Waltham, MA); genomic DNA was isolated using a genomic DNA purification kit (Thermo Fisher Scientific). Quantitative real‐time PCR was performed using the SYBR Premix Ex Taq reagent (Takara, Dalian, China).…”