Consistent grain yield in drought environment has attracted wide attention due to global climate change. However, the important drought-related traits/genes in crops have been rarely reported. Many near-isogenic lines (NILs) of male sterile and fertile Salvia miltiorrhiza have been obtained in our previous work through testcross and backcross in continuous field experiments conducted in 2006–2009. Both segregating sterile and fertile populations were subjected to bulked segregant analysis (BSA) and amplified fragment length polymorphism (AFLP) with 384 and 170 primer combinations, respectively. One out of 14 AFLP markers (E9/M3246) was identified in treated fertile population as tightly linked to the drought stress gene with a recombination frequency of 6.98% and at a distance of 7.02 cM. One of 15 other markers (E2/M5357) was identified in a treated sterile population that is closely associated with the drought stress gene. It had a recombination frequency of 4.65% and at a distance of 4.66 cM. Interestingly, the E9/M3246 fragment was found to be identical to another AFLP fragment E11/M4208 that was tightly linked to the male sterile gene of S. miltiorrhiza with 95% identity and e-value 4 × 10−93. Blastn analysis suggested that the drought stress gene sequence showed higher identity with nucleotides in Arabidopsis chromosome 1–5.

Hereditary multiple exostosis (HME) is an autosomal inherited skeletal disease whose etiology is not fully understood. To further understand the genetic spectrum of the disease, we analyzed a five-generation Chinese family with HME that have observable inheritance. Exome sequencing was performed on three HME individuals and three unaffected individuals from the family. A downstream study confirmed a new C deletion at codon 442 on exon 5 of the exostosin-1 (EXT1) gene as the only pathogenic site which generated a stop codon and caused the truncation of the protein. We rediscovered the deletion in other affected individuals but not in the unaffected individuals from the family. Upon immunohistochemistry assay, we found that the EXT1 protein level of the patients with the novel mutation in our study was less than the level in the patients without the EXT1 mutation from another unrelated family. For a deeper understanding, we analyzed the mutation spectrum of the EXT1 gene. The present study should facilitate a further understanding of HME.

Allergic rhinitis (AR) is a common upper airway disease attributed to a variety of risk factors, such as environmental exposures and genetic susceptibility. The commonly observed comorbidity of asthma and AR in the clinic suggests the presence of shared genetic risk factors and biological mechanisms between these diseases. Interleukin (IL)-33 has been indicated to be an important factor driving asthma susceptibility and pathogenesis using both genome-wide association studies and functional studies in model animals. Although previous studies have reported the putative association of this gene with AR, evidence for the association of genetic variations of IL-33 with the disease is still missing. To examine whether variations in the IL-33 gene confer a genetic risk of AR, a total of 769 patients with AR and 769 age-and sex-matched healthy controls were recruited among Han Chinese residents in the Hubei province, and 14 single-nucleotide polymorphisms (SNPs) spanning the IL-33 gene were examined for their association with the risk of AR. The results indicated that five SNPs, which were in a moderate linkage disequilibrium and were located in the 5'-flanking region of IL-33, exhibited significant associations with the risk of AR, and these associations were additionally supported by genotypic and haplotypic analyses. Notably, three of the five IL-33 SNPs have been previously reported to exhibit genome-wide associations with asthma, and their alleles were also revealed to confer an increased risk of AR in the present study. In summary, the results of the current study suggested that certain variations in the IL-33 gene represent a potential risk for AR, and indicated a shared genetic basis between AR and asthma.

Maize head smut (MHS) caused by the fungi Sporisorium reilianum (Kühn) Landon and Fullerton (S.