A superior allele of the wheat gene TaGL3.3-5B, selected in the breeding process, contributes to seed size and weight.

KEY MESSAGE: A superior allele of wheat gene TaGL3.3-5B was identified and could be used in marker-assisted breeding in wheat. Identifying the main genes which mainly regulate the yield-associated traits can significantly increase the wheat production. In this study, gene TaGL3.3 was cloned from common wheat according to the sequence of OsPPKL3. A SNP in the 8th exon of TaGL3.3-5B, T/C in coding sequence (CDS), which resulted in an amino acid change (Val/Ala), was identified between the low 1000-kernel weight (TKW) wheat Chinese Spring and the high TKW wheat Xinong 817 (817). Subsequently, association analysis in the mini-core collection (MCC) and the recombinant inbred lines (RIL) revealed that the allele TaGL3.3-5B-C (from 817) was significantly correlated with higher TKW. The high frequency of TaGL3.3-5B-C in the Chinese modern wheat cultivars indicated that it was selected positively in wheat breeding programs. The overexpression of TaGL3.3-5B-C in Arabidopsis resulted in shorter pods and longer grains than those of wild-type counterparts. Additionally, TaGL3.3 expressed a tissue-specific pattern in wheat as revealed by qRT-PCR. We also found that 817 showed higher expression of TaGL3.3 than that in Chinese Spring (CS) during the seed development. These results demonstrate that TaGL3.3 plays an important role in the formation of seed size and weight. Allele TaGL3.3-5B-C is associated with larger and heavier grains that are beneficial to wheat yield improvement.

Glucosinolate Profiles in Different Organs of 111 Radish Accessions and Candidate Genes Involved in Converting Glucobrassicin to 4-Hydroxyglucobrassicin.

Glucosinolate (GSL) not only has highly physiological function for plants but also has considerable human interest. We analyzed the GSL compositions and levels in four organs of 111 radish accessions. Seven major GSLs were detected (approximately 5-245 µmol g-1 DW), among which 4-(methylsulfinyl)but-3-enyl GSL and 4-methylsulfanyl-3-butenyl GSL were the dominant GSLs. GSL levels varied substantially among species and groups, and some genotypes/groups with special GSL profiles were identified. The total GSL level was higher in seeds than in sprouts, taproots, and leaves. Additionally, a correlation analysis revealed that seed 4-(methylsulfinyl)but-3-enyl GSL levels were highly correlated with sprout GSL levels. Moreover, a candidate gene (RsCYP81F2.3) encoding an enzyme that catalyzes the conversion of indol-3-ylmethyl GSL to 4-hydroxyindol-3-ylmethyl GSL was identified based on the detection and analysis of three radish accessions with relatively high indol-3-ylmethyl GSL, low 4-hydroxyindol-3-ylmethyl GSL, and 4-methoxyindol-3-ylmethyl GSL levels in their seeds. Our results provide some insights for finding materials and genes relevant for breeding new varieties with ideal GSL compositions and levels.

Hyperbaric oxygen alleviates the activation of NLRP­3­inflammasomes in traumatic brain injury.

Growing evidence has demonstrated that the nucleotide­binding oligomerization domain­like receptor family pyrin domain containing 3 (NLRP­3) inflammasome­mediated inflammatory pathways have been involved in the secondary injury of traumatic brain injury (TBI). In the present study, the authors investigated the effects of hyperbaric oxygen (HBO) therapy on the NLRP­3 inflammasome pathway following TBI. Following the evaluation of motor deficits and brain edema, the therapeutic effects of HBO on interleukin (IL)­1ß and IL­18 expression were assessed, as well as NLRP­3 inflammasome activation following TBI. HBO may improve motor score and reduce brain edema, accompanied with the reduction of IL­1ß and IL­18 during the 7­day observation period. Furthermore, HBO suppressed mRNA and protein expression of NLRP­3­inflammasome components, especially reducing NLRP­3 expression in microglia. Thus, these results suggested that HBO alleviates the inflammatory response in experimental TBI via modulating microglial NLRP­3­inflammasome signaling.