Abstract

Hypersensitivity is a natural defense for plants in response to a variety of pathogens such as viruses, bacteria, fungi and is characterized by a programmed cell death (PCD) accompanied by an accumulation of toxic compounds within the dead cell. Hypersensitive response (HR) is considered a biochemical reaction rather than a structural defense mechanism but can be seen with the naked eye or with a microscope. There are two types of hypersensitive responses: structural and induced. PCD is seen in both structural as well as in induced hypersensitive response. PCD is extreme resistance shown by the plants in which it kills its cells (suicidal death), upon a perception of the pathogen to deprive it of nutritional supply and stops its growth. Cell death plays a central role in innate immune responses in both plants and animals. Apoptosis and autophagy are physiological processes and two forms of biochemical PCD. Induced hypersensitive response comes out when the plant recognizes specific pathogen-produced signal molecules known as elicitors. Recognition of elicitors by the host plants activates an army of biochemical reactions. These reactions include an oxidative burst of reactive oxygen species (ROS), alterations in plant cell wall also including cell wall immunity (CWI) and damage-associated molecular patterns (DAMPs), induction of phytoalexins and synthesis of PR proteins. These all, are comprised under the first line of defense of plants which come into action after recognition of conserved molecules characteristic of many microbes. These are called elicitors and are known as microbeassociated or pathogen-associated molecular patterns (MAMPs or PAMPs). The second line of defense of plants is the recognition of effectors through plant resistance gene products known as R genes, which result in effector-triggered immunity (ETI). This is supported by the gene for gene hypothesis. Avirulence gene encodes a protein which is specifically recognized by genotypes of the host plant harboring the matching resistance genes.

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