Table 1.

Infection process of nematophagous fungi.

Group	Representative Species	Host Recognition	Adhesion	Penetration	Digestion
Nematode-trapping fungi	A. oligospora	Mediated by lectin, proteins on the fungal surface interacting with sugar molecules on the nematode cuticle (GalNAc [57], AOL [58], AofleA [59], AoMad1 [60]), a nematode specific pheromone ascaroside [24], or olfactory mimicry that attracts nematode prey [29].	A physical contact between the trap cells and the nematodes, cell-to-cell communication [61], a group of volatile organic compounds furanone, pyrone, and maltol [62], nitrate [63] and autophagy [64] are required for switching from the saprophytic to the pathogenic stage during trap formation and adhesion.	Fungi pierce the cuticle by forming a penetration tube, with a combination of mechanical pressure and extracellular hydrolytic enzymes, such as serine proteases (PII [65], Aoz1 [55], Ac1 [66], Ds1 [67] Dv1 [68], Mlx [69], Mc1 [70]), collagenase, and chitinase [55].	Nematode content is converted to lipid droplets, these fungi obtain nutrients from the nematodes for their growth and reproduction.
Endoparasitic fungi	Drechmeria coniospora	Obligate parasites, using conidia that are ingested by their host, or by spores that adhere to the cuticle of the host [71].	Adhesive conidia that adhere to the nematode cuticle will form an appressorium that presses firmly against the nematode cuticle. Motile zoospores encyst on the nematode’s surface and germinate to produce the injection tube, to infect nematodes by injecting a sporidium [37].	A combination of enzymatic action and mechanical force, followed by vigorous growth of the trophic hyphae, to invade nematodes [72,73,74].	New conidiophores develop from bulbs at the tips of trophic hyphae inside the cadaver, tightly pressed to the internal surface of the cuticle, preventing leakage of host nutrients, perturbing nematode metabolism, and causing nematode death [75].
Egg- and cyst-parasitic fungi	Pochonia chlamydosporia	Aurovertin D showed strong toxicity and recognition of host [76].	Glycoproteins and appressoria responsible for the adhesion of conidia and hyphae to the eggshell [77].	Proteases and chitinases, e.g., PrC from Clonostachys rosea and Ver112 from Lecanicillium psalliotae [78].	Colonizes the host tissues to obtain nutrients and uses available sugars in the egg as a carbon source [46].
Toxin-producing fungi	Pleurotus ostreatus	Induces paralysis via the cilia of nematode sensory neurons [79].	All developmental stages of C. elegans are sensitive to P. ostreatus. Nematodes become paralyzed upon contacting the P. ostreatus hyphae.	Excess calcium influx and hypercontraction of the head and pharyngeal muscle cells in nematodes.	Toxins cause rapid and systemic necrosis in multiple tissues throughout the organism.
Fungi producers of special nematode-attacking devices	Coprinus comatus; Stropharia rugosoannulata	Sharp projections of the special attack devices, mechanically damage the cuticle of the nematode [41,42].	A penetration peg is formed and penetrates the nematode cuticle via mechanical forces and enzymatic activities.	Hyphae colonize the interior of the nematode and project themselves from the infected nematode.	Need toxin assistance to be successful in their nematicidal role (spiny balls).