TECHNICAL UNIVERSITY OF MOMBASA

DEPARTMENT OF PURE AND APPLIED

SCIENCES
MASTERS OF SCIENCE IN BIOCHEMISTRY
BENARD APIRI
MBC/0005/2022
UNIT NAME: BIOSIGNALLING
UNIT CODE: ABT 5104
SUBMITTED TO: DR.KIBITI
SUBMITTTED ON: 13TH JULY 2022
TASK: CAT 1
a)Discuss the transduction pathway leading to hypersensitive response in

plants(12 marks)

Hypersensitive Response (HR) is a form of cell death often associated with plant resistance to

pathogen infection. It’s a process of plants to prevent invasion of their tissues by pathogens and

controlling diseases.HR can be brought about by a number of pathogens any may be seen after a

number of hours after its contact with the plant. It is mostly dictated by avirulence (avr)gene

that is identified by the plant possessing corresponding resistance (R) gene. Association of the

two resulting to disease is called compatible while if resistance is effective, the association is

termed as incompatible. This specific pathogen identification is common in a number of disease

resistance but not all.

HR is induced by two major steps: i.e , recognition of the pathogen and transduction of the

perceived signal(s) to the effector(s) of cell death. Specific pathogen recognition model supports

that the first event in triggering the HR is the direct recognition of the pathogen avr gene product

by thecorrelating plant R gene product. The first alteration seen is after pathogen recognition are

an oxidative burst which leads to synthesis of Reactive Oxygen Intermediates (ROIs) and rapid

ion fluxes across the plasma membrane( XR).

Superoxide is weakly diffusable and could be dismutated to H2O2 or other diffusable, toxic

ROIs that crosss or damages the plasma membrane. A membrane NADPH oxidase similar to that

in mammalian neutrophils is engaged in the activity. ROIs can also take part give signal via the

profferation of lipid peroxides. The XR is known by its uptake of Ca 2+ and export of Cl-and K+

driven by H+-ATPases which leads to in alkalinization of the cytoplasm that results to cell

death.

Oxidative burst and the XR are likely essential but may not be enough in each system to start up cell death
as evident in Soybean cultured cells and Tobacco leaves..There is little information on the molecular

events following the ealier recognition of the avirulence signal and the initial cellular responses .Genetic

advances have shown usefulness in later analyses of signal transduction pathways leading to HR
Transduction pathways leading to the HR.
 b) Outline the ffectors of cell death in plants(5 marks)

The nature of the effectors of HR is still difficult to track down. Some constituents of the

defense response are potentially toxic for the plant cell (e.g. ROIs, phytoalexins, SA). They

can engage directly in cell death .ROIs can lead to loss of cell integrity and viability owing to

their increased reactivity towards membrane lipids, proteins and nucleic acids. In

addition,Serine and cysteine proteinases and endonucleases are part of a complex machinery

set in motion during the HR. In some plants such as Arabidopsis a major phytoalexin,

camalexin, might be necessary on HR. Nevertheless , some of the induced defense molecules

show up after the signs of cell death and are likely not influencers of HR.

c)outline the protectant mechanisms and anti-cell death

pathways in plants(8 marks)

Most probable ROI protectant mechanisms comprises : anti-oxidant enzymes such as

superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase and

polyubiquitin. Expression of these genes take place concurrently with cell death and H2O2

may take part in their induction. The induction of these protectant process, opposed to the

induction of defense genes and cell death, can be independent of Ca2+ signaling. The

induction of defense genes, cell death and anti-oxidant protectant process are managed by

divergent pathways.

Plants have developed anti cell death pathways that manages cell death to steer clear of

deleterious destructions at tissue level. Theses trails may be contrasting than the ones in

animals since transgenic tobacco plant carrying the Bcl-Xl gene don’t show engineered

response to the TMV virus or to P. syringae functional homologues of animal antic cell

death .dad-1 gene in maize ,rice and Arabidopsis are under study to show its role in HR.The
presence of propagation class cell death control mutants (lsd1 and lls1) gives a substanciative

evidence that anti cell death trails exists in plants lls1 mutant from maize encodes a probable

dioxygenase giving a possibility that this gene is involved in detoxication of oxidized

phenolic compounds like salicyclic acid (SA).SA contribute to death and significant levels of

SA pile up during HR. Therefore ,lis1 could act as a srestrainer of cell death by scavenging

SA.

Generally ,induction of HR needs a number of plant signals produced in the plant plasma

membranes .These signals converges into a few genetically and pharmacologically distinct

pathways .Afterwards ,defense genes ,ROI protectant process and cell death can be

prevailed upon a divergent pathway.