The Gale laboratory studies the molecular mechanisms of morphogenesis
in the opportunistic fungal pathogen, Candida albicans.  C. albicans is the
leading cause of invasive fungal disease in immunocompromised patients,
especially premature infants, the patient population that Dr. Gale
(a neonatologist) is particularly interested in.  The pathogenesis
of C. albicans infections is associated with the ability to change the
morphogenesis program from budding yeast-form growth to filamentous,
hyphal-form growth. C. albicans strains that are unable to make the
transition between these morphogenesis programs are less virulent
in animal- and tissue-based models of candidiasis. In addition, hyphae
exhibit tropisms (the ability to change the direction of growth in response
to environmental stimuli) and these are proposed to facilitate tissue
penetration and invasion during the pathogenesis process.

The Gale laboratory uses molecular and cell biological approaches to dissect
the differences that underlie yeast- and hyphal-form growth and to understand
how the filamentous hypha, in particular, facilitates tissue invasion. Specific
research projects involve identifying and characterizing the role of hyphal
tip-localized polarity proteins in morphogenesis, growth tropisms, and tissue
invasion and virulence using in vitro tissue culture models as well as in vivo
models of candidiasis.  In addition, we have developed a set of vectors that
allow PCR-mediated construction of green, yellow, or cyan fluorescent protein
fusions that facilitate the monitoring of protein co-localization and expression
in C. albicans in real time. Using this tool, we are characterizing the temporal
and spatial localization requirements of polarity proteins throughout the cell
cycle, during the transition between morphologic forms, and with alteration
in hyphal growth direction.

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