Gautier Valérie, Tong Laetitia Chan Ho, Nguyen Tinh-Suong, Debuchy Robert, Silar Philippe
Sorbonne Paris Cité, Laboratoire Interdisciplinaire des Energies de Demain (LIED), University Paris Diderot, 75205 Paris, France.
Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, University Paris-Sud, Université Paris-Saclay, CEDEX, 91198 Gif-sur-Yvette, France.
J Fungi (Basel). 2018 Jul 11;4(3):85. doi: 10.3390/jof4030085.
Filamentous fungi frequently undergo bistable phenotypic switches. Crippled Growth of is one such bistable switch, which seems to rely upon the mis-activation of a self-regulated PaMpk1 MAP kinase regulatory pathway. Here, we identify two new partners of this pathway: PaPro1, a transcription factor orthologous to pro1 and ADV-1, and IDC4, a protein with an AIM24 domain. Both and regulate stationary phase features, as described for the other actors of the PaMpk1 signaling pathway. However, PaPro1 is also involved in the control of fertilization by activating the transcription of the HMG8 and the mating type transcription factors, as well as the sexual pheromones and receptor genes. The roles of two components of the STRIPAK complex were also investigated by inactivating their encoding genes: and . The mutants of these genes were found to have the same phenotypes as and mutants as well as additional phenotypes including slow growth, abnormally shaped hyphae, pigment accumulation and blockage of the zygotic tissue development, indicating that the STRIPAK complex regulates, in addition to the PaMpk1 one, other pathways in . Overall, the mutants of these four genes confirm the model by which Crippled Growth is due to the abnormal activation of the PaMpk1 MAP kinase cascade.
丝状真菌经常经历双稳态表型转换。“生长缺陷”就是这样一种双稳态转换，它似乎依赖于自我调节的PaMpk1丝裂原活化蛋白激酶（MAP激酶）调节途径的错误激活。在此，我们鉴定出该途径的两个新伙伴：PaPro1，一种与Pro1和ADV - 1直系同源的转录因子，以及IDC4，一种具有AIM24结构域的蛋白质。正如PaMpk1信号通路的其他成员所描述的那样，PaPro1和IDC4都调节静止期特征。然而，PaPro1还通过激活HMG8和交配型转录因子以及性信息素和受体基因的转录来参与受精控制。我们还通过使STRIPAK复合体的两个组分的编码基因失活来研究它们的作用：PaCla4和PaMob2。发现这些基因的突变体具有与PaMpk1和PaPro1突变体相同的表型，以及包括生长缓慢、菌丝形态异常、色素积累和接合组织发育受阻在内的其他表型，这表明STRIPAK复合体除了调节PaMpk1途径外，还调节构巢曲霉中的其他途径。总体而言，这四个基因的突变体证实了“生长缺陷”是由于PaMpk1 MAP激酶级联异常激活的模型。
