Avian coccidiosis, caused by protozoan parasites of the genus Eimeria, is a globally prevalent and highly pathogenic disease that poses a serious threat to the poultry industry, resulting in significant economic losses. However, the mechanism by which Eimeria species invade host cells remains unclear. Previous studies have identified rhoptry neck protein 2 (RON2) from Eimeria tenella as a critical factor in host cell invasion, but a comprehensive understanding of the role of EtRON2 in host cell invasion and its relationship with E.
View Article and Find Full Text PDFRecently, a new bacterial disease was detected on cucumber stalks. In order to study the pathogenesis of this disease, the pathogenic bacteria were isolated and identified on the basis of morphological and molecular characteristics, and further analyzed for pathogenicity and antagonistic evaluation. Pathogenicity analysis showed that HlJ-3 caused melting decay and cracking in cucumber stems, and the strain reisolated from re-infected cucumber stalks was morphologically identical to HlJ-3 colonies, which is consistent with the Koch's postulates.
View Article and Find Full Text PDFModern sugarcane, a highly allo-autopolyploid organism, has a very complex genome. In the present study, the karyotype and genome architecture of modern sugarcane were investigated, resulting in a genome assembly of 97 chromosomes (8.84 Gb).
View Article and Find Full Text PDFObjectives: To develop robust variants of L-threonine aldolases (L-TAs), potent catalysts for synthesizing asymmetric β-hydroxy-α-amino acids, it is necessary to identify critical residues beyond the known active site residues.
Results: Through virtual screening, a neglected residue Asn305, was identified as critical for catalytic efficiency. Subsequent site-saturation mutagenesis led to a potent variant N305R which exhibited excellent conversions of 88% (87%) and 80% (94%) for the synthesis of L-threo-phenylserine and L-threo-4-fluorophenylserine respectively.
Glioblastoma (GBM) is uniformly lethal due to profound treatment resistance. Altered cellular metabolism is a key mediator of GBM treatment resistance. Uptake of the essential sulfur-containing amino acid methionine is drastically elevated in GBMs compared to normal cells, however, it is not known how this methionine is utilized or whether it relates to GBM treatment resistance.
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