Plant--> Trichoderma invade

ion fluxes + oxidative burst
deposition of callose synthesis of polyphenols

Next, salicylate (SA)+ jasmonate/ethylene (JA/ET)-signaling

Result: plant will have diff degrees of tolerance to the pathogen invasion

This response describe as JA/ET-mediated induce systemic resistance(ISR)-->resemble the response--> triggered by--> plant growth-promoting rhizobacteria (PGPR)

by formation of appressoria- or papillae-like structures and coiling around host hyphae

At higher doses of Trichoderma

its trigger a SA-mediated systemic acquired resistance (SAR) response(similar to necrotrophic pathogens)

T.virens have low hydrophobin expression will damaged in both hydrophobicity and mycoparaisitism

hydrophobins- able to form a hydrophobic coating on the surface of an object

From implication of

1) mitogen-activated protein kinase (MAPK) from cucumber,and
2) MAPK from T. virens in the molecular cross between plant and Trichoderma

Result: triggering the downstream defense responses

Mycoparasitism is a trait present in all Trichoderma sp. -> can parasitize and kill other fungi.

grows in rhizosphere - capable penetrate int and ext of plant root

Trichoderma Benefits: Abilty derive sucrose / other nutrients from plants

Plants Benefits: Boost immunity against invading pathogen, Improve photosynthetic abilities.

Immune response in plants elicit:

When, Trichoderma produces:

1)Xylanase
2)peptaibols (peptaibiotics with high content
of alpha amino isobutyric acid) like alamethicin and trichovirin II

Some fungus can kill nematodes (bio-nematicides).

Mycoparasitism steps: sensing of host/prey fungus -> attraction -> attachment -> coiling around -> lysis by hydrolytic enzymes work together with other secondary metabolites.

Root interaction: produces auxin in promote root growth and gain colonization by the increases of surface area

PKS/NRPS hybrid enzyme involved in defense
responses in maize

Sm1/Epl1=eliciitor produced by Trichoderma:
Deletion of this Trichoderma gene impairs elicitation of ISR in maize

Monomeric form of Sm1(in a glycosylated state)=essential for elicitation properties.
Non-glycosylated state=susceptible to oxidative-driven dimerization in plants rendering Sm1 inactive as inducer of ISR

Root Penetration: Expansion- like protein and cellulose binding modules & endopolygalucturonase

Seven transmembrane G-protein coupled receptor Gpr1 sense fungal prey because mutation (silencing) grp1 gene cause mycoparasite unable to respond to fungus.

Ligand bind to these receptors activate G-protein cascades.

Deletion of Tga3 G-alpha protein-encoding gene also cause loss of response (sensing).

Some Trichoderma spp. are:

1)Not restricted to outer root tissues
2)Can also live in the plant as ‘‘true’’ endophytes

Endophytic Trichoderma species:

1)Induce transcriptomic changes in plants
2)Protect plants from diseases and abiotic stresses
3)preferentially colonize the surface of glandular trichomes and form appressoria-like structure
4)Uses a ‘‘non-root’’ mode of entry into the plant.

Deletion of adenylate cyclase gene tac1 severely affected T. virens growth and mycoparasitic abilities.

1) Trichoderma sp. secretes cell wall degrading enzymes to break down cell wall -> obtain product (signals to recognise host - to know where and whether it is the host plant).

"Kinase adds phosphate groups (phosphorylation)"

2) Binding of ligand to receptors activate G-protein signaling/ cascades -> downstream MAPK (phosphorylation each step) and cAMP pathway.

3) MAPK activates "cellular processes" by regulation (act as downstream effectors) and further induce (full induction) secretes more cell-wall degrading enzymes and secondary metabolism.

Mycoparasites live with plant roots and living or dead fungal biomass.