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Mushroom-forming fungi frequently encounter competitors during their lifecycle, but their defense mechanisms remain largely unexplored. We studied the response of the mushroom-forming fungus Schizophyllum commune during interaction with the fungal competitors Trichoderma harzianum, Trichoderma aggressivum and Purpureocillium lilacinum and the bacterial competitor Serratia quinivorans. Transcriptomics revealed 632 up-regulated genes in the direct interaction zone, which were enriched in small secreted proteins and transporters. A set of 26 genes were up-regulated during all interactions, indicating a core transcriptomic defense response. In the non-interacting edge of the mycelium of S. commune, there were 154 up-regulated genes, suggesting that there is a systemic response due to a signal that reaches unaffected areas. The GATA zinc finger transcription factor gene gat1 was up-regulated during interaction and a Δgat1 strain displayed increased colonization by T. harzianum. Previously linked to mushroom development, this transcription factor apparently has a dual role. Moreover, 138 genes were up-regulated during both interaction and mushroom development, indicating priming of the defense response during development to prepare the fruiting body for future interactions. Overall, we unveiled a defensive response of S. commune during interaction with fungal and bacterial competitors and identified a regulator of this response., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier GmbH.. All rights reserved.)

RotaTeq is a pentavalent rotavirus vaccine that contains five human-bovine reassortant strains (designated G1, G2, G3, G4, and P1) on the backbone of the naturally attenuated tissue culture-adapted parental bovine rotavirus (BRV) strain WC3. The viral genomes of each of the reassortant strains were completely sequenced and compared pairwise and phylogenetically among each other and to human rotavirus (HRV) and BRV reference strains. Reassortants G1, G2, G3, and G4 contained the VP7 gene from their corresponding HRV parent strains, while reassortants G1 and G2 also contained the VP3 gene (genotype M1) from the HRV parent strain. The P1 reassortant contained the VP4 gene from the HRV parent strain and all the other gene segments from the BRV WC3 strain. The human VP7s had a high level of overall amino acid identity (G1: 95-99%, G2: 94-99% G3: 96-100%, G4: 93-99%) when compared to those of representative rotavirus strains of their corresponding G serotypes. The VP4 of the P1 reassortant had a high identity (92-97%) with those of serotype P1A[8] HRV reference strains, while the BRV VP7 showed identities ranging from 91% to 94% to those of serotype G6 HRV strains. Sequence analyses of the BRV or HRV genes confirmed that the fundamental structure of the proteins in the vaccine was similar to those of the HRV and BRV references strains. Sequences analyses showed that RotaTeq exhibited a high degree of genetic stability as no mutations were identified in the material of each reassortant, which undergoes two rounds of replication cycles in cell culture during the manufacturing process, when compared to the final material used to fill the dosing tubes. The infectivity of each of the reassortant strains of RotaTeq, like HRV strains, did not require the presence of sialic acid residues on the cell surface. The molecular and biologic characterization of RotaTeq adds to the significant body of clinical data supporting the consistent efficacy, immunogenicity, and safety of RotaTeq.

The de-novo synthesis of glycogen is now known to involve a novel class of self-glucosylating protein primers. In mammalian skeletal muscle, glycogenin-1 is the protein responsible for this initiation step. Northern blot analysis revealed that glycogenin-1 gene transcription is differentially regulated in the C2C12 mouse muscle cell line. To define the regulatory elements that control expression of the glycogenin-1 gene, we have cloned and characterized the genomic structure of the human glycogenin-1 gene and its promoter region. This gene consists of seven exons and six introns, and spans over 13kb. Transcription of human glycogenin-1 is initiated at two major sites, 80 and 86bp upstream from the initiation of translation codon. Nucleotide sequence analysis of 2.1kb of the 5'-flanking region revealed the proximal promoter contains both a TATA box and two putative Sp1 binding sites located in a CpG island. There are numerous binding sites for developmental and cell-type-specific transcription factors, including AP-1, AP-2, GATA, and several potential Oct 1 binding domains. There are also nine consensus E-boxes that bind the basic helix-loop-helix family of muscle-specific transcription factors. The transcriptional activity of the glycogenin-1 gene was investigated by transient transfection of the 5'-flanking region in HepG2 cells and C2C12 myoblasts and myotubes. These results permitted the definition of a minimal 232bp promoter fragment that is responsible for basal level transcription in a cell-type-independent manner. Furthermore, we have identified a regulatory region located between -2076 and -1736 of the 5'-flanking region of the human glycogenin-1 gene that allows myotube-specific expression in C2C12 cells.