Identification and characterization of extrachromosomal circular DNA in the silk gland of Bombyx mori

The silk gland cells of silkworm are special cells which only replicate DNA in the nucleus without cell division throughout the larval stage. The extrachromosomal circular DNAs (eccDNAs) have not yet been reported in the silk gland of silkworms. Herein, we have explored the characterization of eccDNAs in the posterior silk gland of silkworms. A total of 35 346 eccDNAs were identified with sizes ranging from 30 to 13 569 549 bp. Motif analysis revealed that dual direct repeats are flanking the 5′ and 3′ breaking points of eccDNA. The sequences exceeding 1 kb length in eccDNAs present palindromic sequence characteristics flanking the 5′ and 3′ breaking points of the eccDNA. These motifs might support possible models for eccDNA generation. Genomic annotation of the eccDNA population revealed that most eccDNAs (58.6%) were derived from intergenic regions, whereas full or partial genes were carried by 41.4% of eccDNAs. It was found that silk protein genes fib-H, fib-L, and P25, as well as the transcription factors SGF and sage, which play an important regulatory role in silk protein synthesis, could be carried by eccDNAs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that the genes carried by eccDNAs were mainly associated with the development and metabolism-related signaling pathways. Moreover, it was found that eccDNAfib-L could promote the transcription of fib-L gene. Overall, the results of the present study not only provide a novel perspective on the mechanism of silk gland development and silk protein synthesis but also complement previously reported genome-scale eccDNA data supporting that eccDNAs are common in eukaryotes.

Microstructure characterization and HCF fracture mode transition for modified 9Cr-1Mo dissimilarly welded joint at different elevated temperatures

The high cycle fatigue（HCF） tests of modified 9 Cr-1 Mo dissimilarly welded joint were carried out at different elevated temperatures and the fracture mechanism was systematically revealed. The fatigue strength at 108 cycles based on S-N curve can be estimated as a half of weld joint＇s yield strength for all conducted temperatures, which can be a reliable criterion in predicting the fatigue life. The results show that the inter-critical heat affected zones（IC-HAZs） of both sides are the weak zones due to their low hardness and inferior fatigue resistance property. HAZ of COST-FB2（BM2） is the weakest zone at room temperature due to the existence of numerously distributed defects and the initiation of cracks, either in the surface or interior zone, impacting a crucial effect on the fatigue life of the joint. While at elevated temperatures, fatigue life was controlled mostly by the intrusion-extrusion mechanism at the specimen surface under high stress level and subsurface non-defect fatigue crack origin（SNDFCO） from the interior material under low stress amplitude. With increasing temperature, more and more fatigue failures began to occur at the HAZ of COST-E（BM1） due to its higher susceptibility of temperature. Besides, it is found that the-ferrite in the BM1 has no harm to the HCF behavior of the joint at the conducted temperatures.

Modification Mechanism and Uniaxial Fatigue Performances of A356.2 Alloy Treated by Al-Sr-La Composite Refinement-Modification Agent

Modification mechanism and uniaxial fatigue properties of A356.2 alloy treated by Al-6Sr-7La and traditional Al-5Ti-1B/Al-10Sr(hereinafter refers to traditional treated alloy) were investigated by constant stress amplitude method. Microstructure, dislocation and Si twinning of the alloys were studied by thermal analysis, scanning electron microscopy(SEM) and transmission electron microscopy(TEM). The results showed that Al-6Sr-7La possesses better refining and modification effect than Al-5Ti-1B/Al-10Sr. Meanwhile, fatigue properties of the alloy treated by Al-6Sr-7La are higher than traditional treated alloy, and this is mainly owing to that Al-6Sr-7La treated alloy has more twins in eutectic Si and lower twin spacing. In addition, higher density of nanophases formed on twin faces and La-rich clusters appear at multiple twin intersections. Stacking faults and entrapped nanophases appeared on growing Si twin faces. Impurity induced twinning(IIT) mechanism and twin plane re-entrant edge(TPRE) mechanism are valid for eutectic Si which are important for mechanical optimization of A356.2 alloy.

Ribosomal protein S26 serves as a checkpoint of T-cell survival and homeostasis in a p53-dependent manner

Ribosomal proteins(RPs),which play critical roles in ribosome assembly and protein translation,have been proven to be associated with important physiological and pathological processes,including the regulation of T-cell development and immune-related diseases.1,2,3 A recent study reported that ribosomal protein S26(Rps26),which is a Diamond–Blackfan anemia-associated RP located in the 40S subunit that controls oocyte growth,4,5 may influence multiple different immune phenotypes.6 Moreover,a SNP in the 5′UTR of the Rps26 gene in CD4^(+)and CD8+T cells was implicated in several autoimmune diseases.7 However,the function of Rps26 in T lymphocytes remains unknown.Here,we found that Rps26 was highly expressed in T lymphocytes.We examined a T-cell-specific Rps26 knockout mouse model and reported for the first time that ablation of Rps26 in T cells not only impairs peripheral T-cell homeostasis but also leads to T-cell developmental arrest in the thymus.Mechanistically,Rps26 critically regulates T-cell survival in a p53-dependent manner.These findings reveal the indispensable role of the Rps26-p53 axis in T-cell development and homeostasis.

Intrinsic PD-L1 promotes antitumor activity of CD8^(+)cytotoxic T lymphocytes via in cis interaction with CD80

Dear Editor,Programmed cell death-ligand 1(PD-L1)on tumor cells can inhibit CD8+cytotoxic T lymphocyte(CTL)-mediated antitumor response by trans-engagement with programmed death protein 1(PD-1).Besides tumor cells,PD-L1 is expressed on T cells.However,the intrinsic role of PD-L1 in T cells has not been widely studied.PD-L1 expression is essential for the survival of activated CD8+T cells,and PD-L1 blockade at the contraction stage reduced the number of effector T cells[1].CD8+T cell responses to influenza virus infection were also impaired in PD-L1-deficient mice[2].