Disease relevance of actA

• Methods for curing endogenous prophages from the comK attachment site in 10403S-derived strains were developed. pPL1 was used to introduce the hly and actA genes at comK-attBB' in deletion strains derived from 10403S and SLCC-5764 [1].
• Listeria monocytogenes Mutants Carrying Newcastle Disease Virus F Gene Fused to its actA and plcB: In vitro Expression and Immunogenicity in Chickens [2].
• Evidence implicating the 5' untranslated region of Listeria monocytogenes actA in the regulation of bacterial actin-based motility [3].
• We addressed the impact of antivector immunity, elicited by immunization with attenuated actA-deficient Listeria monocytogenes, on the CD8(+)-T-cell response to a well-characterized lymphocytic choriomeningitis virus epitope, NP118-126, delivered by infection with recombinant L. monocytogenes [4].

High impact information on actA

• The transposon had inserted in actA, the second gene of an operon [5].
• To investigate the interaction of ActA with the microfilament system in the absence of other bacterial factors, the listerial actA gene was expressed in eukaryotic cells [6].
• In this study, an in-frame deletion mutation within the actA gene was constructed and introduced into the L. monocytogenes chromosome by allelic exchange [7].
• Upon infection with actA-deficient LM, macrophages and microglial cells rapidly, and later LM-specific CD4 and CD8 T cells, produced TNF [8].
• The analysis of Ag presentation by macrophages and dendritic cells isolated from spleens of infected mice revealed efficient presentation of L. monocytogenes-derived CD4 T cell epitopes that was not dependent on the actA-mediated intercellular spread of bacteria [9].

Biological context of actA

• Analysis of sequence data for 120 L. monocytogenes isolates revealed evidence of clustering between isolates from the same source, based on the phylogenies inferred from actA and inlA (P = 0.02 and P = 0.07, respectively; SourceCluster test) [10].
• The resulting mutant isolates displayed a wide range of actA expression levels, and many were less sensitive to environmental signals that normally mediate repression of virulence gene expression [11].
• Bacterial actin assembly requires expression of the bacterial gene actA [12].
• To identify bacterial factors that participate in the intracellular induction of actA expression, L. monocytogenes mutants expressing high levels of actA during in vitro growth were selected after chemical mutagenesis [11].
• We employed a germfree (GF) mouse model to try to accentuate the development of a humoral mucosal immune response in the gut, and we used oral colonization with one of the mutants, actA-negative (DeltaactA) L. monocytogenes, to restrict infection largely to the gut [13].

Anatomical context of actA

• Definitive evidence for the role of ActA was provided by showing that a actA-complemented DeltaActA mutant was restored in its capacity to invade fetuses [14].
• The actA locus of L.monocytogenes encodes a 90 kDa polypeptide that is a key component of bacterium-host cell microfilament interactions [15].
• In contrast, mice immunized with a low dose of actA-deficient L. monocytogenes had approximately 10-fold fewer effector and memory T cells specific for LLO91-99 and a substantially higher CD8(+)-T-cell response against the recombinant antigen after challenge with recombinant L. monocytogenes [4].
• Collectively, these results indicate that the dramatic induction of actA expression that occurs in the host cell cytosol is mediated through a single promoter element [16].
• Expression of actA in Listeria innocua was sufficient to promote entry of this non-invasive species into epithelial cell lines, but not into COS-1 and Hepa 1-6 cells, indicating that ActA directs an internalization pathway specific for epithelial cells [17].

Associations of actA with chemical compounds

• We have constructed 20 clustered charged-to-alanine mutations in the NH2-terminal domain of ActA and replaced the endogenous actA gene with these molecular variants [18].
• A chloramphenicol resistance assay indicated that the hly fusion but not the actA fusion was significantly activated in Luria-Bertani (LB) broth, and this finding correlated with LLO and ActA levels detectable in broth cultures [19].
• The actA gene of isolate H4 had deletions of 105 nucleotides corresponding to 35 amino acid deletions falling within the proline-rich region [20].

Regulatory relationships of actA

• Finally, in comparison to induction in broth cultures, actA was highly induced (226-fold) and hly was moderately induced (20-fold) in J774 cells [19].

Other interactions of actA

• Microvilli played an active role in the phagocytosis of the prfA* strain, and actA was required for their remodelling into pseudopods mediating bacterial uptake [17].
• Phylogenetic analyses of partial sigB and actA sequences showed that lineage III represents three distinct subgroups, which were termed IIIA, IIIB and IIIC [21].

Analytical, diagnostic and therapeutic context of actA

• We have used immunocytochemistry to show that the actA gene product, ActA, is distributed asymmetrically on the bacterial surface: it is not expressed at one pole and is increasingly concentrated towards the other [12].
• A total of 133 Listeria monocytogenes isolates were characterized by ribotyping and allelic analysis of the virulence genes hly, actA, and inlA to uncover linkages between independent phylogenetic and specific virulence markers [22].
• CONCLUSIONS: The developed 5'-nuclease PCR of the actA gene provides a new target for the rapid detection and quantification of L. monocytogenes [23].
• Sequence analysis of the actA gene of Listeria monocytogenes isolated from human [24].

References