Soll D R
Curr Top Med Mycol. 1985;1:258-85. doi: 10.1007/978-1-4613-9547-8_10.
By analyzing the effects of zinc on growth and dimorphism, it has become clear that there exists at least two modes, or "pathways," of mycelium formation in C. albicans (7). Paradoxically, even though the characteristics for the two modes appear to be opposite in nature, the mycelium that form appear to be superficially similar. Unfortunately, it may be difficult to compare the two modes unambiguously at the molecular level for two reasons. First, the physiology of cells resuming growth after release from stationary phase will undoubtedly differ drastically from the physiology of cells exiting from the growth cycle, regardless of phenotype. Therefore, most molecular or physiologic differences probably will represent differences in growth rate or position in the cell cycle, rather than alternate molecular mechanisms that are basic to the alternate modes of mycelium formation. Second, it has been observed that during release from stationary phase, a prescribed program of gene expression accompanies commitment to the mycelial and budding forms (11). This program was demonstrable because of the excellent synchrony and homogeneity of released cultures (60), which is a characteristic lacking in cultures entering stationary phase in the M10 mode. Even so, a comparison at the molecular level between the two modes of mycelium formation should be undertaken with the above reservations in mind. Perhaps the most attractive aspect of alternate modes of mycelium formation in Candida is at the genetic level of analysis. The hypothesis of homozygosis in the expression of the M10 phenotype is testable, as is the possible role of the M10 phenotype in tissue penetration. If the hypothesis is true and if the M10 phenotype predominates in infected tissue, it would represent a new mechanism of opportunism in infectious fungi that may be used by other systems as well as Candida. If it is not true, a detailed analysis of the differences between the two modes of mycelium formation will still be valuable in our understanding of both the mechanisms regulating phenotypic transitions in Candida and the more general question of cell divergence in developing systems.
通过分析锌对生长和二态性的影响，已明确白色念珠菌中至少存在两种菌丝体形成模式或“途径”(7)。矛盾的是，尽管这两种模式的特征在本质上似乎相反，但形成的菌丝体表面上却很相似。不幸的是，由于两个原因，在分子水平上明确比较这两种模式可能很困难。首先，无论表型如何，从稳定期释放后恢复生长的细胞的生理学无疑将与退出生长周期的细胞的生理学有很大差异。因此，大多数分子或生理差异可能代表生长速率或细胞周期位置的差异，而不是菌丝体形成替代模式所基于的替代分子机制。其次，已经观察到，在从稳定期释放期间，伴随着对菌丝体和芽殖形式的定向，会有一个规定的基因表达程序(11)。由于释放培养物具有出色的同步性和同质性(60)，这个程序是可证明的，而这是在M10模式下进入稳定期的培养物所缺乏的特征。即便如此，在进行两种菌丝体形成模式的分子水平比较时，应牢记上述保留意见。也许念珠菌菌丝体形成替代模式最吸引人的方面在于遗传分析层面。M10表型表达中的纯合性假说以及M10表型在组织穿透中的可能作用都是可以检验的。如果该假说正确且M10表型在感染组织中占主导地位，那么它将代表感染性真菌中一种新的机会主义机制，其他系统以及念珠菌可能也会利用这种机制。如果该假说不正确，对两种菌丝体形成模式之间差异的详细分析对于我们理解念珠菌中调节表型转变的机制以及发育系统中更普遍的细胞分化问题仍将是有价值的。
