Affect of Phytohormons in Leaf Senescence

7/31/2019 Affect of Phytohormons in Leaf Senescence

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IN THE NAME OF GOD

LEAF SENESCENCEDepartment of plant biotechnology

Guilan university

Presentation: F.masoomi-aladizgehMail: [email protected]


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Senescence is the age-dependent deterioration process at thecellular, tissue, organ, or organismal level, leading to death or theend of the life span.

During senescence, leaf cells undergo rather orderly changes incell structure, metabolism, and gene expression.

The earliest and most significant change in cell structure is thebreakdown of the chloroplast, the organelle that contains up to70% of the leaf protein.

Increased catabolic activity is responsible for converting thecellular materials accumulated during the growth phase of leafinto exportable nutrients that are supplied to developing seeds orto other growing organs.


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Arabidopsis thaliana is the best modelfor genetic studying

Arabidopsis thaliana is a favorite model for themolecular genetic study of leaf senescence.

It has a short life cycle. Its leaves undergoreadily distinguishable developmental stages.

It has one of the smallest genomes in theplant kingdom: 115,409,949 base pairs ofDNA distributed in 5 chromosomes (2n = 10).

It can be easily grown in the lab in arelatively small space.


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Development is rapid. It only takes 5 6 weeks fromseed germination to the production of a new crop ofseeds.

It is a prolific producer of seeds(up to 10,000 per plant) makinggenetics studies easier.

It is normally self-pollinated sorecessive mutations quicklybecome homozyguos and thusexpressed.

It almost has a 25,498genes, butthe scientist have not located allgenes yet.


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Leaf senescence associated cell death asa programmed cell death

Programmed cell death (PCD) is a self-destructingcellular process triggered by external or internal factorsand mediated through an active genetic program.

Cell death does not occur coherently but starts with local

patches of early-dying cells and then propagates into thewhole-leaf area.

A few examples of PCD in plants are observed:

I. It is in the pathogen-induced hypersensitive response(HR).

II. It is in terms of the biological function, PCD in leafsenescence is mostly for remobilization of nutrients fromthe leaf to other organs including developing seeds.

III. Its role in germination-related degeneration of aleuron.


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Structural and Biochemical Changes inLeaf Senescence-Associated Cell Death

A notable feature of cellular structural change during leafsenescence is the order ofdisintegration of intracellularorganelles.

The earliest structural changes occur in the chloroplast, Incontrast, the nucleus and mitochondria that are essentialfor gene expression and energy production, respectively,remain intact until the last stages of senescence.

The overall cellular content of polysomes and ribosomesdecreases fairly early, reflecting a decrease in proteinsynthesis. This occurs concomitantly with reduced synthesisof rRNAs and tRNAs and mRNAs.


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The senescence markers: chlorophyll content

Photochemical efficiency

senescence-associated enzyme activities

change ofprotein levels

membrane ion leakage

Gene expression

RNase or peroxidase activity


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Leaf senescence is accompanied by decreased expressionof genes related to photosynthesis (CAB2) and proteinsynthesis (RPS, RBC) and by increased expression ofsenescence-associated genes (SAGs).

Microarray analysis,RT-PCR, ESTs and

RNA gel blotanalysis can indicatecontents of gene expression.


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Factors involved in leafsenescence

There are two factors:

1) Internal factors(include various phytohormones and reproductivedevelopment as well as developmental age).

2) External factors(include stresses such as high or low temperature, drought,

ozone, nutrient deficiency, pathogen infection, and

shading.)


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1

Internal factors

Hormones

Cytokinin

Ethylene

Auxin

JA

ABA

SA

GA

Reproduction

External factors

Abiotic

UV-B or ozone

Nutrient limitation

Heat or cold

Drought

Biotic

Shading

Pathogen attack

or wounding

Regulatory

network

Developmentalage

Macromolecule

degradation

Nutrient salvage

& translocation

Detoxification

& defense

Chlorophyll loss/ nitrogen and lipid mobilization Increase of antioxidants and defense-related genes

Cell death

DNA laddering/ disruption of the nucleus and mitochondria

Disintegration of the plasma and vacuolar membranes


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Involvement of Phytohormone Pathways inLeaf Senescence

The hormonal pathways appear to play at all the stagesof leaf senescence, including the initiation phase ofsenescence, progression, and the terminal phases.

Each plant hormone affects various developmentaland/or environmental events in a complex manner. Thiscauses difficulties in assaying the roles of the hormonalpathways in leaf senescence.


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Cytokinin:

The endogenous cytokinin level drops during leafsenescence and exogenous application or endogenousenhancement of cytokinin content using the senescence-

specific SAG12 promoter delays senescence.

The genes involved in cytokinin synthesis, a cytokininsynthase and adenosine phosphate isopentenyl-transferase (IPT) genes, are downregulated and a genefor cytokinin degradation, cytokinin oxidase, isupregulated in senescing leaves.


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Ethylene:

ethylene is an important positive regulator of leafsenescence.

The ethylene biosynthetic genes encoding ACC synthase,ACC oxdiase, and nitrilase are upregulated in senescing

leaves.

Arabidopsis mutants, ethylene-resistant 1 (etr1) andethylene-insensitive 2 (ein2),that are deficient in ethylene

perception and signal transduction, respectively, exhibitedsignificant delays in leaf senescence.


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In transgenic Arabidopsis and tomato plants thatconstitutively overproduce ethylene do not exhibitearlier-onset leaf senescence, suggesting that ethylenealone is not sufficient to initiate leaf senescence.

The old1 mutant displays a phenotype with earlier-onsetsenescence in an age-dependent manner.

The early-senescence phenotype was further acceleratedby exposure to ethylene, showing that the old1 mutationresulted in alternation ofboth of the age- and ethylenesignaling dependent leaf senescence.

i h ld d bl h h l i


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However, in the old1etr1double mutant where ethylene perceptionwas blocked by the mutation in the ETR1 gene, age-dependentearlier-onset leaf senescence still occurred but was not furtheraccelerated by ethylene treatment.


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Abscisic acid(ABA):

The ABA level increases in senescing leaves andexogenously applied ABA induces expression of several

SAGs.

In some stress conditions ABA content increases in leaves,because the genes encoding the key enzyme in ABA

biosynthesis, 9-cisepoxycarotenoid dioxygenase (NECD),and two aldehyde oxidase genesAAO1andAAO3showincreased expression.


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ABA also induces expression ofantioxidant genes andenhances the activities ofantioxidative enzymes such assuperoxide dismutase (SOD),ascorbate peroxidase(APOD), and catalase (CAT).

A recent report argued that ABA induces accumulation ofH2O2 in senescing rice leaf, which in turn accelerates leafsenescence.


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Methyl jasmonate (MeJA):

Methyl jasmonate (MeJA) and its precursor JA promotesenescence in detached oat (Avena sativa) leaves.

Exogenously applied MeJA to detachedArabidopsis leaves leads toa rapid loss of chlorophyll content and photochemical efficiency ofphotosystem II (PSII) and increased expression ofSAGs such asSEN4, SEN5, and VPE.

They observed that JA-dependent senescence is defectivein the JA-insensitive mutant coronatine insensitive 1(coi1),implying that the JA signaling pathway is requiredfor JA to promote leaf senescence.


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Salicylic asid(SA):

A recent intriguing discovery in leaf senescence was therole ofSA in age-dependent leaf senescence.

The concentration of endogenous SA is four times higherin senescing leaves ofArabidopsis.

Leaves from Arabidopsis pad4 mutants that are defectivein the SA signaling pathway do not appear to undergo celldeath as efficiently as the wild type.

SA involved in upregulation of several SAGs during leafsenescence such as PR1a, chitinase, and SAG12


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Gibberellin asid(GA):

it has been reported that the gibberellins can retard leafsenescence.

In 17 species studied, only Taraxacumn officinailedemonstrated a gibberellic acid regulation of senescence.

Therefore, GA is the hormone that negatively regulatesthe leaf senescence.


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IAA:

The auxin level increases during leaf senescence. Consequently,IAA biosynthetic genes encoding tryptophan synthase (TSA1),IAAld oxidase (AO1), and nitrilases (NIT1-3) are upregulated

during age-dependent leaf senescence.

Exogenous application of auxin represses transcription of someSAGs.

This implies that the auxin level increases during leaf senescencedue to increased expression of auxin biosynthetic genes, which leadsto delayed leaf senescence.


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Disruption ofARF2 by T-DNA insertion causes delay inleaf senescence. The phenotype canonically puts ARF2 asa positive regulator of leaf senescence.

Besides the regulatory genes mentioned above, severalother regulatory genes of leaf senescence have beenidentified such as:DLS1, ORE1, ORE7, ORE9, SOR12

AUXIN RESPONSE FACTOR 2 (ARF2) is one of the transcriptionrepressors in the auxin signaling pathway. Microarray analysisshows that expression of the ARF2 gene is induced in senescingleaves.


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Division of phytohormones:

Enhancers for SAG

expression

Inhibitors for SAG

expression

Ethylene

ABA

MeJA

SA

Cytokinin

IAA

GA


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Conclusion:

With the aid ofmicroarray, we now know that more than 800genes are distinctively upregulated during senescence, whichillustrates the dramatic alteration in cellular physiology that

underlies leaf senescence.

It is also unlikely that all the cells within an individual leafundergo coherent cell death. To better understand thesenescence process, it will be necessary to develop assays

that can monitor senescence symptoms and senescence-associated cell death symptoms at the individual cellularlevel.


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Refrence:

Pyung Ok Lim, Hyo Jung Kim, and HongGil Nam

Department of Science Education, Cheju NationalUniversity, Jeju, Jeju, 690-756, Korea

Division of Molecular Life Sciences and National Core ResearchCenter for Systems Bio-Dynamics, POSTECH, Pohang, Kyungbuk,

790-784, Korea;email: [email protected]


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Affect of Phytohormons in Leaf Senescence