Yao Shuangyan, Feng Yuting, Islam Amjad, Shrivastava Manjari, Gu Hongcheng, Lu Yumeng, Sheng Jiaqi, Whiteway Malcolm, Feng Jinrong
Department of Pathogen Biology, School of Medicine, Nantong University, Nantong 226001, Jiangsu, China.
Nantong Health College of Jiangsu Province, Nantong 226010, Jiangsu, China.
Comput Struct Biotechnol J. 2020 Dec 1;18:4002-4015. doi: 10.1016/j.csbj.2020.11.034. eCollection 2020.
The polymorphous cellular shape of , in particular the transition from a yeast to a filamentous form, is crucial for either commensalism or life-threatening infections of the host. Various external or internal stimuli, including serum and nutrition starvation, have been shown to regulate filamentous growth primarily through two classical signaling pathways, the cAMP-PKA and the MAPK pathways. Genotoxic stress also induces filamentous growth, but through independent pathways, and little is known about negative regulation during this reversible morphological transition. In this study, we established that in , similar to its homolog in , has a role in nuclei separation and spindle orientation. Deletion of generated filamentous and invasive growth as well as increased biofilm formation, accompanied by up-regulation of hyphae specific genes, such as , and . The filamentous and invasive growth of the deletion strain was independent of transcription factors Efg1, Cph1 and Ume6, but was suppressed by deleting checkpoint or overexpressing . Deletion of impaired the colonization of cells in mice and also attenuated virulence in a mouse model. All the data suggest that loss of activates filamentous and invasive growth , and that it positively regulates virulence , which provides insight into actin-related morphology and pathogenicity in .
尤其是从酵母形态转变为丝状形态的多形细胞形状，对于宿主的共生或危及生命的感染至关重要。各种外部或内部刺激，包括血清和营养饥饿，已被证明主要通过两条经典信号通路，即cAMP-PKA和MAPK通路来调节丝状生长。基因毒性应激也会诱导丝状生长，但通过独立的通路，并且对于这种可逆形态转变过程中的负调控知之甚少。在本研究中，我们确定在[具体物种名称]中，与其在[另一物种名称]中的同源物类似，在细胞核分离和纺锤体定向中发挥作用。[具体基因名称]的缺失产生了丝状和侵袭性生长以及生物膜形成增加，同时伴随着菌丝特异性基因如[具体基因名称]上调。[具体基因名称]缺失菌株的丝状和侵袭性生长独立于转录因子Efg1、Cph1和Ume6，但通过缺失检查点[具体名称]或过表达[具体名称]受到抑制。[具体基因名称]的缺失损害了[具体物种名称]细胞在小鼠中的定殖，并且在小鼠模型中也减弱了毒力。所有数据表明，[具体基因名称]的缺失激活了丝状和侵袭性生长，并且它正向调节毒力，这为[具体物种名称]中与肌动蛋白相关的形态和致病性提供了见解。
