We previously demonstrated that genes encoding a putative two-component histidine kinase (response regulator (candidiasis and that strains with each gene deleted are also defective in morphogenesis under certain growthconditions. In the present study, the role of these two genes in the adherence to and colonization of reconstitutedhuman esophageal tissue (RHE) is described. We compared strains of CHK1) or aCSSK1) are each required for virulence in a murine model of hematogenously disseminatedCandida albicans with deletions ofchk1 (strain CHK21) and cssk1 (strain CSSK21) to wild-type cells (CAF2), as well as strains with CHK1 andCSSK1 evaluated in periodic acid-Schiff-stained sections, as well as by SEM. We observed that both deletion-containingstrains colonized the RHE to a lesser extent than did CAF2 and that the percent germination by bothstrains was reduced in comparison to that of control strains at 1 h postinfection. Expression of reconstituted (strains CHK23 and CSSK23, respectively). Adherence and colonization of RHE wereCHK1 or CSSK1was quantitated by reverse transcription (RT)-PCR from RHE tissues infected with wild-type cells. Expression of both although expression of of indicating that pathways. Our observations indicate that conversion to filamentous growth on RHE tissue.C. albicans yeastCHK1 and CSSK1 increased over the 48-h period following infection of the tissue,CHK1 was greater than that of CSSK1. By RT-PCR, we have also shown that expressionCHK1 and CSSK1 in the strains with cssk1 and chk1 deleted, respectively, was similar to that of CAF2,CHK1 and CSSK1 do not regulate each other but probably encode signal proteins of differentCHK1 and CSSK1 are each partially required for colonization and