Biomedical Engineering Reference
In-Depth Information
adhere equally if one, two, or all of these genes are activated/non-activated?
The answer to these questions may confi rm the need or redundancy of
these genes and may also shed light on the sequential involvement of these
genes in the optimal adhesion/interaction of C. albicans with its contact
surface (plastic or cell/tissue surfaces). Adhesion is not the only process
that involves multiple genes.
Pmt2 is highly sollicited for C. albicans growth and PMT1 is essential
for hyphal morphogenesis. IPT1 also contributes to the hyphal form of
C. albicans . Adhesion, growth and form changes are involved in biofi lm
formation. PMT1 and IPT1 genes are thus involved in biofi lm formation
and potentially, in C. albicans virulence. This raises questions regarding their
sequence and the order of intervention/action of each gene in this virulence.
Are they all required to promote C. albicans growth, morphological hyphal
changes and biofi lm formation? Which gene is activated fi rst during each
process (growth, morphological changes, biofi lm formation)?
We must also bear in mind that some C. albicans genes may have
antagonistic effects. Indeed, contrary to PMT and IPT, ADH1 was shown
to reduce the formation of biofl ims. The answers to these questions may
demonstrate that C. albicans genes that are apparently regulated during
adhesion, growth, morphological changes and infection processes may not
truly be required for Candida virulence. Further investigations of the specifi c
function/involvement of each gene on C. albicans physiology/virulence
will certainly contribute to the development of stronger, more effi cient
antifungal molecules, which will be a major challenge in the near future.
ACKNOWLEDGMENTS
Data presented in this chapter were supported by grants from the
NIH/R01-DE017486-01A1 and BRS-ACURE Q0600136 (Oral HIV/
AIDS Research Alliance, OHARA (MAG) and the Natural Sciences and
Engineering Research Council of Canada (NSERC) Discovery Program
(MR).
REFERENCES
Akpan, A. and R. Morgan R. 2002. Oral candidiasis. Postgrad. Med. J . 78: 455-9.
Arendorf A.T. and D.M. Walker. 1980. The prevalence and intra-oral distribution
of Candida albicans in man. Arch. Oral Biol . 2: 507-538.
Becker, P., W. Hufnagle, G. Peters and M. Herrmann. 2001. Detection of differential
gene expression in biofilm-forming versus planktonic populations of
Staphylococcus aureus using micro-representational-difference analysis. Appl.
Environ. Microbiol . 67: 2958-2965.
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