Disease relevance of mpl

• In vitro transcription of the Listeria monocytogenes virulence genes inlC and mpl reveals overlapping PrfA-dependent and -independent promoters that are differentially activated by GTP [1].

High impact information on mpl

• Direct frequency analyses of immune splenocytes, however, revealed that LLO 91-99 and p60 217-225 elicit dominant T cell responses, while p60 449-457 and mpl 84-92 elicit minor, subdominant responses [2].
• The life-time of the prfA, plcA, and mpl transcripts is short [3].
• The entire mpl gene was cloned in a plasmid able to replicate in L. monocytogenes [4].
• The maturation of the 33-kDa proenzyme to the 29-kDa phosphatidylcholine phospholipase C (PC-PLC) of Listeria monocytogenes requires the production of the zinc metalloprotease encoded by mpl, the proximal gene of the lecithinase operon [4].
• The most discriminatory 600-bp fragments identified in the housekeeping and stress response genes differentiated the isolates into 8 to 10 subtypes; intergenic region sequences yielded 8 and 12 allelic types based on 335- and 242-bp sequences for hly-mpl and plcA-hly, respectively [5].

Other interactions of mpl

• Synthesis of p60 in L. monocytogenes was significantly lower when the iap gene was placed under the control of the actA or the mpl promoter [6].

Analytical, diagnostic and therapeutic context of mpl

• It was suggested that PCR detection of genes prfA, mpl, or plcB may not be sufficient to detect virulent strains of L. monocytogenes [7].

References