## 6 Conclusions  
The ability to adapt is essential for filamentous fungi and yeast to survive and proliferate under non-optimal osmotic environments. Fungi sense and then transduce external changes in osmotic pressure mainly through cellular signaling pathways such as the HOG pathway that is mediated by MAPK cascades. Activated MAPKs phosphorylate a number of substrates including transcriptional activators that in turn modulate patterns of gene expression and subsequent protein synthesis. In fungi, responses to osmotic stress include the production of osmoprotectant compounds such as glycerol, reorganization of the cytoskeleton, and cell wall biogenesis. A fungus' response to high osmotic pressures in an artificial environment such as during an industrial fermentation that utilizes controlled environmental and nutritional parameters is fairly straightforward. However, during a host-fungal pathogen interaction, the degree to which a fungus' response to changes in osmotic pressure impacts its ability to successfully invade and survive in the host is not so clear. During the infection process, a pathogenic fungus would be expected to encounter a complex nutritional milieu upon lysis of plant cells that may include increased osmotic pressure. The entomopathogenic fungus, _Metarhizium anisopliae_, kills insects by direct penetration of the cuticle followed by multiplication in the hemolymph. The solute-rich hemolymph is characterized by high osmotic pressure [88] that could initiate a stress response in the fungus. _M. anisopliae_ strains that were defective in the MOS1 osmosensor (SHO1 in yeast) displayed increased sensitivity to osmotic pressure as well as reduced virulence against larvae of _Manduca sexta_[89]. In the case of a plant necrotic ph fungus, the breakdown of cell walls by fungal hydrolases and the generalized hypersensitive response by the host plant may result in the invading fungus being isolated in a region of high osmotic pressure. In addition, activation of the Hog1 MAPK pathway has been observed in _Candida albicans_ cells exposed to the human antimicrobial peptide, histantin 5 [90]. It is possible that antimicrobial compounds elicited by the host may also trigger activation of the osmotic stress response in an invading plant or human pathogenic fungus leading to accumulation of osmolytes such as glycerol and reorganization of cell wall structure in an attempt to stave off death. With the ever increasing number of organisms whose genomes and proteomes have now been sequenced and annotated, it should be possible to better elucidate the impact that genes involved in the osmotic stress response have on host-fungal pathogen interactions.  
The literature cited in this review indicates that the osmoadapatative response is conserved but not identical in different fungi and that it is intimately linked to morphogenesis. The ability to alter morphogenic programs in response to changes in osmotic pressure can play a significant role in the fungus' capacity to survive and flourish in nature. One developmental response to an increase in osmotic stress often observed in fungi is an increase in conidial. This increases the fungus' chances of survival as conidia can be dispersed by wind over wide areas thus removing the fungus from an inhospitable environment and potentially allowing it to take up residence in a more favorable environment. Furthermore, some of the studies mentioned in this review have also shown that in some cases the response to osmotic stress by fungi is linked to the biosynthesis of natural products, including mycotoxins. However, examples of this are few and more studies will be necessary to gain further insight into the interaction between osmotic stress regulation and secondary metabolism.