Agropyron cristatum (2n = 4x = 28, PPPP), which harbours many high-yield and disease-resistance genes, is a promising donor for wheat improvement. Narrow genetic diversity and the trade-off between grain weight and grain number have become bottlenecks for increasing grain yield in wheat. In this study, a novel translocation line, WAT650l, was derived from the chromosome 6P addition line 4844–12, which can simultaneously increase both grain number per spike (GNS) and thousand-grain weight (TGW). Cytological analysis and molecular marker analysis revealed that WAT650l was a 5BL·5BS-6PL (bin 12–17) translocation line. Assessment of agronomic traits and analysis of the BC4F2 and BC5F2 populations suggested that the 6PL terminal chromosome segment in WAT650l resulted in increased grain number per spike (average increased by 14.07 grains), thousand-grain weight (average increased by 4.31 g), flag leaf length, plant height, spikelet number per spike and kernel number per spikelet during the two growing seasons of 2020–2021 and 2021–2022. Additionally, the increased GNS locus and high-TGW locus of WAT650l were mapped to the bins 16–17 and 12–13, respectively, on chromosome 6PL by genetic population analysis of three translocation lines. In summary, we provide a valuable germplasm resource for broadening the genetic base of wheat and overcoming the negative relationship between GNS and TGW in wheat breeding.
ABSTRACT The high molecular weight glutenin subunits (HMW‐GS) are essential in determining bread‐making quality, and knowing their composition can help in making appropriate decisions to improve wheat ( Triticum aestivum L.) quality. The HMW‐GS compositions of 189 Chinese wheat landraces (CWLs), 61 introduced lines (ILs), and 840 Chinese improved varieties (CIVs) were investigated by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis (SDS‐PAGE) in this study. The aim was to identify novel HMW‐GS alleles and to compare the genetic diversity among the three groups. A total of 31 HMW‐GS alleles and 86 allele combinations were found in all accessions. For CWL and CIV, the predominant pattern was (null, 7+8, 2+12), with a frequency of 71.6 and 26.0%, respectively. The predominant pattern in the IL was (null, 7+9, 2+12) with a frequency of 13.6%. The IL had the largest variation and the average index of genetic variation (H). The H was 0.6117, whereas CWL and CIV had H values of 0.2275 and 0.5161, respectively. In addition, the present study showed that an increase of 7+9 and 5+10 in the CIV came from the use of foreign parents. The results revealed that the IL was an important reservoir for improving Chinese wheat‐quality characteristics such as grain protein content, hardness, and sodium dodecyl sulfate (SDS) sedimentation. Although the genetic variation in the CWL was low, it contained novel alleles (1Bx7.1* and 1By8.1*), which indicated that this group was also a potential resource for wheat‐quality improvement.
The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in the majority of tumor cells, whilst sparing normal cells. However, the potential use of TRAIL in the treatment of cancer is limited by the inevitable emergence of drug resistance. The present study reports the upregulation of latent membrane protein 1 (LMP1)-induced TRAIL resistance via the enhanced expression of X‑linked inhibitor of apoptosis protein (XIAP) in nasopharyngeal carcinoma (NPC) cells. LMP1‑positive NPC cells were indicated to be more sensitive to TRAIL compared with LMP1-negative NPC cells in three NPC cell lines. CNE‑1 is a LMP1‑negative NPC cell line that was transfected with pGL6-LMP1; following which, sensitivity to TRAIL decreased. LMP1‑induced TRAIL resistance was associated with the decreased cleavage of caspase‑8,‑3 and ‑9, BH3 interacting domain death agonist (Bid) and mitochondrial depolarization, without any effects on the expression of the death receptors, B‑cell lymphoma (Bcl)‑2 and Bcl-extra long. Knockdown of XIAP with small interfering RNA increased caspase‑3 and ‑9 and Bid cleavage, and prevented LMP1‑induced TRAIL resistance. Furthermore, embelin, the inhibitor of XIAP, prevented LMP1‑induced TRAIL resistance in the Epstein‑Barr virus (EBV)‑positive CNE‑1‑LMP1 and C666‑1 NPC cell lines. However, embelin did not enhance TRAIL‑induced apoptosis in NP‑69, which was used as a benign nasopharyngeal epithelial cell line. These data show that LMP1 inhibits TRAIL‑mediated apoptosis by upregulation of XIAP. Embelin may be used in an efficacious and safe manner to prevent LMP1‑induced TRAIL resistance. The present study may have implications for the development and validation of novel strategies to prevent TRAIL resistance in EBV-positive NPC.
To determine the distribution and influence of lysosomal neuraminidase (Neul), protective protein/cathepsin A (PPCA) and beta-galactosidase (beta-gal) in the inner ear of the mouse, and to observe their auditory alterations in enzyme deficiency.Six wild type (2 months postnatal) (Neu1+/+, PPCA+/+ and beta-gal+/+) mice were used, and Neu1, PPCA and beta-gal homozygous (Neu1-/-, PPCA-/- and beta-gal-/-) mice at the same age used as control in this experiment. The auditory thresholds were examined through the auditory brainstem responses (ABR) to click, which tone pips were 8, 16, and 32 kHz. The mice were intracardically perfused with 4% paraformaldehyde. The bulla were further fixed in 4% paraformaldehyde, processed and sectioned with paraffin embedded method. Immunohistochemistry was used to determine the cellular localizations of Neu1, PP-CA, and beta gal in the inner ear.There was a similar distributive pattern of Neu1, PPCA and betagal in the inner ear. Neu1 intense staining was observed in the cochlear spiral ganglion cells, spiral limbus, spiral ligament, vestibular ganglion cells, cristae, maculae hair cells, and weak staining in inner hair cells, outer hair cells, supplying cells of the organ of Corti and stria vascularis. The intense staining of PPCA and beta-gal were observed in the spiral ganglion and vestibular ganglion cells, and weak staining in the spiral limbus, spiral ligament, stria vascularis and organ of Corti. The inner ear exhibited no staining when Neul, PPCA and beta-gal were deficient, respectively. A positive staining of PPCA and beta-gal was presented in Neu1-/- mice, and as well as Neu1 and PPCA in beta-gal-/- mice. However, the staining of Neu1 was not presented, and only very weak staining of beta-gal in PPCA-/- mice. The auditory thresholds of Neul, PPCA, and beta-gal mice were elevated for 60-69 dB, 40-48 dB, and 7-10 dB above those of wildtype littermates, respectively.Neu1 PPCA and beta-gal are distributed in the inner ear of mouse, and the three enzymes also form a lysosomal multi-enzyme complex in the inner ear. The respective enzyme deficiencies can induce the hearing the loss of different levels.
To observe the alterations of the auditory function and morphology of the ear in the mouse sialidosis models which has been generated by targeted deletion of lysosomal neuraminidase gene (Neul) and closely resembled the phenotypes in corresponding human conditions, and to explore pathophysiological mechanisms of hearing impairment.Neul homozygous (Neul -/-) mice at 3 weeks, 2 and 4 months of age, and their wildtype littermates (Neu1 +/+) were examined for auditory thresholds through auditory brainstem responses (ABR) to click, 8, 16, and 32 kHz stimuli. Morphological analyses in ears were performed by series temporal bone section and light microscopy.Neul -/- mice at 3 weeks of age showed an elevated ABR threshold, 50-55 dB above those of Neul +/+ mice. Up to 2 and 4 months of age, their thresholds were further elevated for 60-68 dB. There were distinct pathological changes of middle and inner ear of 3 weeks of age in Neul -/- mice, especially at 2-4 months of age there were significant cerumen occlusion in the external auditory canal and severe otitis media. Vacuolation associated with lysosomal storage was observed within ossicles and cochlear bone cells, stria vascularis cells, spiral ganglion neurons and macrophages, spiral limbus, spiral prominence, Reissner's membrane cells, and the mesothelial cells of the perilymphatic scala and basilar membrane, but not within the organ of Corti. Vestibular ganglion neurons, hair cells and supporting cells in cristae and maculae also showed vacuolation.The deficiency of lysosomal neuraminidase may result in a serious hearing loss and morphological alterations of ear. The external auditory canal obstruction, otitis media and ossicle changes may cause conductive hearing loss, and the defects in lysosomal storage of neurons, stria vascularis, spiral limbus, Reissner's membrane and basilar membrane cells may contribute to sensorineural deafness.
Grain number per spike (GNPS) is a major factor in wheat yield breeding. The development of high GNPS germplasm is widely emphasized in wheat-yield breeding. This paper reported two high GNPS wheat germplasm lines, Pubing 3228 and Pubing 3504, which had a stable and wide adaptability to different ecological regions. By exploring a nested cross design with reciprocals using Pubing 3228 or Pubing 3504 as a common parent and investigating the GNPS phenotypes of F1 hybrids in 2007-2008 and F2 populations in 2008-2009 of different cross combinations, the narrow-sense GNPS heritability was up to 49.58 and 52.23%, respectively. Genetic model analysis predictions suggested that GNPS in Pubing 3228 and Pubing 3504 was mainly controlled by additive genetic effects. Correlation analysis results between GNPS and 1 000-kernel weight (TKW) of F2 populations showed that TKW was not influenced with the increase of GNPS. The good coordination among three yield components of spike number per plant (SNPP), GNPS, and TKW in the F2 segregating population implied that selection of good candidate individuals in breeding programs would be relatively straightforward. Overall, our results indicated that Pubing 3228 and Pubing 3504 are two potential germplasm lines for yield improvement of GNPS in pedigree selection of wheat breeding.