Figure 12.

An overview of proteins and pathways activated and targeted by PemK_Sa toxin in C. elegans. PemK_Sa is sequence-specific endoribonuclease recognizing the tetrad sequence UAUU mRNA and cut it between U and A nucleotides. Chances are that PemK_Sa in present study might targeted the codon of Tyrosine and anticodon of Isoleucine UAU, it either degrade the mRNA or stopped the protein synthesis, or generate mutated proteins which lack the native confirmation. Toxins are directly targeting the host cell mitochondria and blocks the voltage gated channels and other important pores. Inhibition of glycolysis will also decrease coenzyme NADH and FADH which act as reduced powers and inhibit the ETC. PemK_Sa might be blocking synaptic nicotinic receptor and affect or degenerate the C. elegans neurons. Phosphatidylinositol 3,4,5-trisphosphate (PIP3), is a component of cell membrane that activates numerous signaling pathways resulting in cell proliferation, growth, survival, glucose transport and protein synthesis. Glycogen synthase kinase-3 (GSK-3), a serine-threonine kinase, is an important component of the glycogen metabolism pathway. It is highly expressed in neurons for development and repair which activates ubiquitin-protease for degradation. GSK-3 inhibiting phase II gene expression in the oxidative stress defense. Inhibition or blockage of voltage gated Na²⁺, Ca²⁺, and K²⁺ channels play a critical role in the generation and propagation of action potentials in neurons and muscle cells. Protein kinase C (PKC-1) phosphorylates a range of cellular proteins. Which acts as an extracellular signal regulated mitogen-activated protein kinase (ERK/MAPK), in response to diverse sensory neurons. Its role in regulation differs depending on the neuron in which it is acting. Required for incomplete resistance to antimitotic toxins. In C. elegans an increased ROS, H₂O₂ and expression of other oxidant proteins activates innate immunity and anti-oxidant proteins for toxin inactivation.