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Abstract: Attempts were made to establish one-step multiplex PCR assay for the identification of the widely used species in deer products (sika deer, wapiti, red deer and reindeer). Primers were designed from tandem repeat region of D-loop and well-conserved region of 16S rDNA after alignment of the available sequences in the GenBank database. The primers generated specific fragments of 307bp in length for sika deer, 307 and 246bp for wapiti, 272bp for Tarim red deer, 230bp for red deer and 141bp for reindeer, respectively. The detection limit was 0.05ng for sika deer and wapiti, 0.1ng for Tarim red deer, 0.5ng for red deer and 0.02ng for reindeer. The results demonstrated that the fraudulent phenomenon is epidemic in the substitution of deer products, in especially antler, penis, foetus and tendon products. Hence, this multiplex PCR provided a useful and sensitive technique to identify the sources of deer products. [Copyright &y& Elsevier]

ArgR, a transcriptional regulator belonging to the AraC/XylS family, plays a key role in arginine metabolism regulation. ArgR has also been found to repress the transcription of a lipase gene, but its molecular mechanism is still unknown. In this study, we investigated the molecular mechanism acting on the expression of intracellular lipase gene lipA regulated by ArgR in Pseudomonas protegens Pf-5 through knockout and overexpression of argR , detection of DNA-protein interaction in vivo , determining whole-cell lipase activities of various strains derived from Pf-5, and examining β-galactosidase activities of various lacZ fusions. The results demonstrated that ArgR inhibits lipA expression at the transcriptional level. Further results showed that the inhibition of lipA transcription by ArgR is mediated by binding to the ArgR binding site of lipA promoter to produce steric hindrance, in which the common sequence, TGTCGC is crucial for the ArgR binding. Besides, arginine inhibits lipA expression in both wild-type and argR mutant, and shows a synergistic inhibition on lipA expression when combined with ArgR. To the best of our knowledge, this is the first report on ArgR directly repressing the transcription of a lipase gene. • ArgR directly inhibits lipA transcription by binding to lipA promoter. • lipA promoter includes an ArgR binding site bound by ArgR. • Arginine represses lipA expression in both wild-type and argR knockout mutant. [ABSTRACT FROM AUTHOR]