Abstract
Viruses employ an array of elaborate strategies to overcome plant defense mechanisms and must adapt to the requirements of the host translational systems. Pokeweed antiviral protein (PAP) from Phytolacca americana is a ribosome inactivating protein (RIP) and is an RNA N-glycosidase that removes specific purine residues from the sarcin/ricin (S/R) loop of large rRNA, arresting protein synthesis at the translocation step. PAP is thought to play an important role in the plant’s defense mechanism against foreign pathogens. This review focuses on the structure, function, and the relationship of PAP to other RIPs, discusses molecular aspects of PAP antiviral activity, the novel inhibition of this plant toxin by a virus counteraction—a peptide linked to the viral genome (VPg), and possible applications of RIP-conjugated immunotoxins in cancer therapeutics.
Highlights
An evolutionary arms race between plants and their pathogens has shaped each other’s elaborate strategies for survival
It was not established until several years later that the inhibition of protein synthesis was due to the impairment of host ribosomes [21]
Cytotoxicity of ribosome inactivating protein (RIP) and their effects on biological systems present the investigators with novel ideas in exploration of new pathways for the inhibition of RIP
Summary
An evolutionary arms race between plants and their pathogens has shaped each other’s elaborate strategies for survival. Many plants produce toxic proteins that are thought to play a key role in their defense mechanisms against foreign pathogenic invaders. These anti-pathogenic protein toxins are known as ribosome inactivating proteins (RIPs). High toxicity of the castor (Ricinus communis) and jequirity (Abrus precatorius) bean plants owe their detrimental physiological effects toward eukaryotic cells to these poisons and have been known since antiquity [1]. Other plants (e.g., common pokeweed—Phytolacca americana and common soapwart—Saponaria officinalis) produce pokeweed antiviral protein (PAP) [12] and saporin [13], respectively, with increased antiviral and antifungal activities. It is hypothesized that they gain access into the cytoplasm as the pathogen enters the cell, promoting their activity by impairing host ribosomes [16]
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