## 1 Introduction  
Infection often begins with adherence. Microbes attach to host cells, tissues, or implanted devices, and then engage in pathogenic interactions such as invasion or inflammation. For many infectious microbes, the mechanisms that coordinate attachment and pathogenesis are well characterized. For example, in the case of enteropathogenic and enteroahemorrhagic _Escherichia coli_, the injected bacterial Tir protein mediates both bacterial attachment and host cytoskeletal rearrangements that ultimately lead to pathological effects [1]. In the case of _Helicobacter pylori_, contact with gastric epithelial cells induces formation of pili that translocate pathogenic effectors into host cells [2]. The pathogens _Yersinia pestis_ and _Candida albicans_ express invasin proteins that promote both attachment to and entry into host cells [3; 4]. Because mechanisms that coordinate adherence and attachment are linchpins of infection, they provide insight into pathogenicity functions, and also present potential therapeutic targets. Our focus is the fungus _C. albicans,_ which is responsible for diverse mucosal and disseminated infections [5]. This organism can grow as ovoid yeast cells, cylindrical hyphal cells, and other cell types [6; 7]. Hyphae express numerous surface adhesins that mediate adherence to host cells and abiotic surfaces [8; 9; 10]. Adherence thus establishes a foothold for invasion and biofilm formation. Hyphae from biofilms, on either mucosal or abiotic substrates, invade the underlying surface [11]. There are two modes of hyphal invasion. The first mechanism depends upon host cell functions: _C. albicans_ hyphae induce their own endocytosis via the surface invasins Als3 and Ssa1 [9; 12; 13]. These invasins stimulate the actin-mediated endocytic pathway through interaction with E-cadherin and EGFR/HER2 on the epithelial surface [13, 14]. The second mechanism is host cell-independent: _C. albicans_ hyphae may invade a cell or substrate through exertion of force. This mechanism has been revealed through analysis of hyphal growth behaviors on abiotic surfaces [11, 15]. Force-mediated invasion has been well studied in the plant pathogenic fungi _Magnaporthe oryzae_ and _Colletotrichum graminicola_[16, 17, 18, 19]. These fungi form a special melanized cell structure, the approximium, which initiates invasion after adherence to the host surface. The approximium generates enormous turgor via glycerol accumulation that drives a penetration peg through an underlying leaf surface [16]. It seems reasonable that _C. albicans_ might also rely upon glycerol accumulation to generate turgor. Glycerol has a prominent role in _C. albicans_ biofilm formation, as first shown by [PERSON] and colleagues [20]. They found that the glycerol biosynthetic gene _RHR2_, which specifies 3-phosphoglycerphosphatase, is up-regulated in biofilm cells compared to planktonic cells. This gene expression relationship reflects function, because they found that an _rhr2l/l_ deletion mutant is defective in biofilm formation _in vitro_. Direct measurements have confirmed that _C. albicans_ biofilm cells accumulate higher levels of glycerol than planktonic cells [21, 22]. We confirmed the studies of [PERSON] and colleagues, and extended the observations to show that _RHR2_ is required for biofilm formation _in vivo_ in a catheter infection model [21]. The functional role of _RHR2_ was unexpected, though: we observed that an _rhr2l_ mutant has reduced adherence to a silicone substrate, and that it is defective in expression of biofilm adhesin genes [21]. Expression of adhesin genes such as _ALS1_ from an _RHR2_-independent promoter permitted biofilm formation of an _rhr2l/l_ mutant _in vitro_ and _in vivo_. This observation indicated that the major role of _RHR2_ in biofilm formation is to promote adhesin gene expression. Here we have explored the function of _RHR2_ under two other conditions: an _in vitro_ surface invasion model, and an _in vivo_ intra-abdominal candidiasis (IAC) model.