Germination of Microsporidian Spores: The Known and Unknown

Abstract

Microsporidia are a large group of mysterious obligate intracellular eukaryotic parasites. The microsporidian spore can survive in the absence of nutrients for years under harsh conditions and germinate within seconds under the stimulation of environmental changes like pH and ions. During germination, microsporidia experience an increase in intrasporal osmotic pressure, which leads to an influx of water into the spore, followed by swelling of the polaroplasts and posterior vacuole, which eventually fires the polar filament (PF). Infectious sporoplasm was transported through the extruded polar tube (PT) and delivered into the host cell. Despite much that has been learned about the germination of microsporidia, there are still several major questions that remain unanswered, including: (i) There is still a lack of knowledge about the signaling pathways involved in spore germination. (ii) The germination of spores is not well understood in terms of its specific energetics. (iii) Limited understanding of how spores germinate and how the nucleus and membranes are rearranged during germination. (iv) Only a few proteins in the invasion organelles have been identified; many more are likely undiscovered. This review summarizes the major resolved and unresolved issues concerning the process of microsporidian spore germination.

New insights into the effects of UV light on individual Nosema bombycis spores, as determined using single‐cell optical approaches

“…In addition to ionic strength, the major factors affecting germination are the proteins on the spore wall, pH, osmotic pressure and temperature. 43 The findings herein revealed that UV radiation affects Nb germination in two ways. First, irradiation decreases the germination rate and reduces the number of germinable spores.…”

“…Once inside the host, the spores germinate and release their infectious contents, resulting in the establishment of the parasite within the host's cells. 42,43 The results of this study suggest that disrupting the permeability of the spore wall to allow trehalose leakage or altering the induction of spores to germination stimuli, thereby preventing spore germination, are mechanisms by which UV radiation acts on Nb spores, both of which are effective ways to stop Nb spore infection and ideas for developing new disinfection methods and controlling silk diseases.…”

“…13,14,[29][30][31] However, the germination of Nb spores is not related to nucleic acids, but is an intricate process involving stimulated signal transduction and the extrusion of polar filaments. 42,43 The signal transduction pathway and underlying molecular mechanisms still remain poorly understood, but the mechanisms that trigger polar filament ejection and sporoplasm extrusion are relatively clear. 43 The spores are activated by stimuli and absorb a large amount of water, thereby creating intracellular pressure, which is transferred to the posterior polar vesicles after reaching a certain level.…”

“…42,43 The signal transduction pathway and underlying molecular mechanisms still remain poorly understood, but the mechanisms that trigger polar filament ejection and sporoplasm extrusion are relatively clear. 43 The spores are activated by stimuli and absorb a large amount of water, thereby creating intracellular pressure, which is transferred to the posterior polar vesicles after reaching a certain level. As the posterior pole vesicles expand, the polar filaments begin to protrude, gradually unscrew and form a tube, which is ejected from the pole cap.…”

E. hellemSer/Thr protein phosphatase PP1 targets the DC MAPK pathway and impairs immune functions

“…As a result, the existence of pathogen-derived PP1 within host cells may be of great importance for both pathogen cells’ intracellular proliferation and host cell manipulation. As for microsporidia, many species have been proved to possess this proteinase and exert important functions, for example, in germination ( 48 , 49 ). Our study is the first and very excited one to identify the E. hellem -derived serine/threonine PP1 and verify the direct interaction with host p38α (MAPK14) in the MAPK signaling pathway.…”