Congresos y reuniones científicas
Título:
STAPHYLOCOCCAL -TOXIN INDUCES ACTIVATION AND DEGRADATION OF C-JUN AND JUN D TRANSCRIPTION FACTORS
Autor/es:
ALEJANDRO J MOYANO; RACCA AC; ANDREOLI, VERONICA; CLAUDIA SOLA; G PANZZETA-DUTARI; BOCCO, JOSE LUIS
Reunión:
Congreso; Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y. Biología Molecular (SAIB-2012); 2012
Institución organizadora:
Sociedad Argentina de Investigación en Bioquímica y. Biología Molecular
Resumen:
displays a large set of virulence factors,
amongwhich the pore-forming -toxin has been shown to be crucial
in the establishment of severe and often fatal infections such as
necrotizing pneumonia.However, itsmolecularmechanisms are not
well understood. In the present study we evaluated the role of c-Jun
and JunD, two transcription factors of the AP1 complex which are
key regulators of cell fate upon diverse stimuli, including microbial
infections. Western blot analysis as well as immunofluorescence
studies showed a strong a-toxin-induced phosphorylation of c-Jun
and JunD with a concomitant decrease of their protein levels. The
use of pharmacological inhibitors showed that this phosphorylation
was dependent on the JNK signaling pathway. On the other hand,
inhibition of p38 and ERK increased the c-Jun and JunD protein
levels. Furthermore, pretreatment with the MG132 proteasome
inhibitor showed that this pathway contributed to the a-toxin-
dependent degradation of c-Jun and JunD. In addition, Real-Time
PCR revealed that c-Jun was also downregulated at transcriptional
level. Finally, knockdown of c-Jun by siRNA showed that this
protein contributed to the host cell survival against a-toxin. These
results shed light on the nuclear response orchestrated by c-Jun and
JunDduring cell stress triggered by staphylococcal a-toxin.
Staphylococcus aureus