Disease relevance of CHS7

• Here, it is shown that most chitin synthesis in Candida albicans, one of the fungi most commonly isolated from opportunistic mycoses and infections, depends on CHS7 [1].

High impact information on CHS7

• Chs3 palmitoylation is required for ER export, but not for interaction with its dedicated ER chaperone, Chs7 [2].
• Chs7p, a new protein involved in the control of protein export from the endoplasmic reticulum that is specifically engaged in the regulation of chitin synthesis in Saccharomyces cerevisiae [3].
• In addition, chs7 null mutants show the yeast phenotypes associated with a lack of chitin: reduced mating efficiency and lack of the chitosan ascospore layer, clear indications of Chs7p function throughout the S. cerevisiae biological cycle [3].
• However, only the class IV CHS genes chs7 and chs5 are crucial for shaping yeast cells and hyphae ex planta [4].
• Candida albicans strains deficient in CHS7, a key regulator of chitin synthase III, exhibit morphogenetic alterations and attenuated virulence [1].

Other interactions of CHS7

• Overexpression of GFA1 caused an approximately threefold increase in chitin in the transformed cells, whereas chitin content was barely affected by the joint overexpression of CHS3 and CHS7 [5].
• In the absence of CHS7 product, Chs3p, but not other secreted proteins, is retained in the ER, leading to a severe defect in CSIII activity and consequently, to a reduced rate of chitin synthesis [3].
• F. oxysporum chs1-, chs2- and chs7-deficient mutants were constructed through targeted gene disruption by homologous recombination [6].
• EhCHS-1 is deposited chitin in the lateral wall of transformed Saccharomyces cerevisiae Chs mutants, independent of accessory proteins (Chs4p to Chs7p) required by yeast Chs3p [7].

References