Kuliah 10_Senesence dan Penyakit Tumbuhan

  Senescence dan Penyakit Tumbuhan

Senescence and cell death are normal, actively controlled processes

  Reproductive senescence Nutritional senescence Pathogen-induced cell death Developmental cell death Autumnal senescence _{Photos courtesy Gunawardena, A.H.L.A.N., Greenwood, J.S. and Dengler, N.G. (2004). Programmed cell death remodels lace plant leaf shape during} Senescence is a slow process of nutrient reassimilation followed by death

  Senescence is a process by which nutrients are remobilized into seeds (annual plants) or bark and other tissues of long-lived plants

  Senescence:

• is an active developmental program that requires upregulation of many genes
• is not simply necrosis or death by neglect

Programmed cell death (PCD)

  Programmed cell death (PCD) is an active process to remove unneeded or damaged cells. Breakthroughs in our understanding came from studies of C. elegans, culminating in the Nobel Prize in Medicine in 2002

  Programmed cell death is a normal developmental program that removes cells from between the digits and inside the intestinal lumen Examples of plant PCD

  Death during defense Death during development PCD is a developmental program

in many tissues

  Leaf senescence Tracheary element formation Aerenchyma formation Self incompatibility

  Sepal and petal senescence Organ abortion in unisexual flowers

  Hole development in lace plant leaf Extra embryos

  Suspensor Adapted from Gadjev, I., Stone, J.M., and Gechev, T.S. (2008) Programmed cell death in plants: new insights into redox regulation and the role of hydrogen peroxide. Int. Rev. Cell Mol, Biol. 270: ; _{Reprinted by permission from Macmillan Publishers Ltd Filonova, L.H., von Arnold, S., Daniel G., and Bozhkov, P. V. (2002) Programmed cell death eliminates all but one embryo in a polyembryonic plant seed.} 

  Root cap cells Tracheary element formation in Zinnia elegans cells is a model for PCD

  Lacayo, C.I., Malkin, A.J., Holman, H.-Y.N., Chen, L., Ding, S.-Y., Hwang, M.S. and Thelen, M.P. (2010). Imaging cell wall architecture in single Zinnia elegans tracheary

  Mesophyll cell Tracheary element

  Isolated mesophyll cells can form tracheary elements in culture, allowing identification of genes involved in PCD

  Mesophyll cell Procambial cell

  Dedifferentiation Secondary wall deposition PCD Tracheary element

  

Elongation

Defensive cell death

  The hypersensitive response (HR) is a defensive response. Infected cells and adjacent cells are killed through PCD _{Reprinted by permission from Macmillan Publishers Ltd Lam, E. (2004) Controlled cell death, plant survival and}

Leaf senescence: Death as a recycling process

  Developmental Environmental signals signals Decrease in Disassembly of Cell death cellular contents and photosynthesis, activation of degradation of macromolecules senescence program

  Developmental senescence In monocarpic plants, reproduction triggers senescence.

  Monocarpic plants flower once, set seed and die.

  Most crop plants are monocarpic

  

Photoperiod induces leaf

senescence in autumn leaves

Bhalerao, R., Keskitalo, J., Sterky, F., Erlandsson, R., Björkbacka, H., Birve, S.J., Karlsson, J., Gardeström, P., Gustafsson, P., Lundeberg, J., and Jansson, S. (2003). Gene expression in

  Day length is the signal that initiates leaf senescence, but the rate at which senescence occurs

  is affected by temperature Autumn senescence is a relatively slow process Drought and other stresses induce leaf senescence

Hormones may contribute differently to different types of senescence

  

Reprinted with permission from Buchanan-Wollaston, V., Page, T., Harrison, E., Breeze, E., Lim, P.O., Nam, H.G., Lin, J.-F., Wu, S.-H., Swidzinski, J., Ishizaki, K. and Leaver, C.J. (2005).

^{Reproduction Metabolism Stress}

  There seem to be multiple pathways leading to the induction of senescence

The onset of senescence brings about a change in gene expression

  Visible Expansion Maturity

  Necrosis senescence

  No gene

  Genes

  expression

  sorted by

  after death

  temporal patterns of expression

  Senescence associated genes (SAGs)

  From Buchanan-Wollaston, V. (1997). The molecular biology of leaf senescence. Journal of Experimental Botany. 48: s adapted in

Proteins encoded by SAGs reveal senescence processes

  Days after sowing Breeze, E., et al., and Buchanan-Wollaston, V. (2011). High-resolution temporal profiling of transcripts during

Chlorophyll degrades during senescence

  The first visible sign of leaf senescence is chlorophyll breakdown In some plants this is accompanied by unmasking of

  carotenoids or

  accumulation of

  anthocyanins, turning _{Woo, H.R., Chung, K.M., Park, J.-H., Oh, S.A., Ahn, T., Hong, S.H., Jang, S.K. and Nam, H.G. (2001). ORE9, an F-Box protein that regulates leaf} leaves orange or red.

Carotenoids and anthocyanins absorb and dissipate excess light energy

• Chl

  Anthocyanin accumulation in palisade cells of sugar maple

• Chl + anthocyanin

  Pre-senescent: Light is absorbed and drives photosynthesis

  Mechanisms of senescence - summary

  Leaf senescence has many triggers Different hormones are involved in different types of senescence, and different sets of genes are induced _{signalling pathways between developmental and dark/starvation-induced senescence in Arabidopsis. Plant J. 42: 567-585. Swidzinski, J., Ishizaki, K. and Leaver, C.J. (2005). Comparative transcriptome analysis reveals significant differences in gene expression and} Reprinted with permission from Buchanan-Wollaston, V., Page, T., Harrison, E., Breeze, E., Lim, P.O., Nam, H.G., Lin, J.-F., Wu, S.-H., Economic impacts of senescen ce

  Senescence-induced Wild type - Wild type - cytokinin synthesis - Drought Stressed

  Well Watered Drought Stressed

  Delaying senescence can enhance drought tolerance

Timing of senescence affects yield and grain quality

  From Uauy, C., Distelfeld, A., Fahima, T., Blechl, A. and Dubcovsky, J. (2006). A NAC gene regulating senescence Delayed senescence

  Delaying senescence increases total photosynthesis and can increase grain yields

  However, delaying senescence can also reduce mobilization of nutrients into the seeds, lowering their quality

  

Senescence affect post-harvest

food quality

  Harvesting can

  Broccoli – five days post- harvest Broccoli – day of harvest

  induce senescence, particularly in broccoli and asparagus

  How can food-shelf-life be enhanced?

• •Cold temperatures

• Low oxygen-environment
• Ethylene removal or ethylene insensitivity
• Increased cytokinin synthesis or responsiveness
• Other genetic methods to delay senescence

  Petal senescence affects a $100

billion industry

  How much more would you pay for roses guaranteed to stay pretty for two or more weeks?

  Petal senescence in Ipomoea nil (morning glory)

Yamada, T., Ichimura, K., Kanekatsu, M. and van Doorn, W.G. (2009). Homologs of genes associated with programmed cell death in animal cells are differentially expressed during senescence of Ipomoea nil petals.

_{Plant Cell Physiol. 50: 610-625; Yamada, T., Ichimura, K. and van Doorn, W.G. (2006). DNA degradation and nuclear degeneration during programmed cell death in petals of Antirrhinum, Argyranthemum, and}

  The biochemistry of senescence in petals is similar to that in leaves

Death and Senescence - Summary Death matters:

  From embryogenesis to senescence, programmed cell death is essential for plant fitness and viability

  Understanding death and senescence is important:

  As we learn more about these processes we decrease food losses to stress and disease, and enhance yields and quality of food and ornamental plants

Senescence and Plant Disease

  Many plant pathogens show interactions with host development.

  Pathogens may modify plant development according to their nutritional demands.

  

Conversely, plant development influences pathogen growth.

Biotrophic pathogens often delay senescence to keep host

cells alive, and resistance is achieved by senescence-like processes in the host.

  Necrotrophic pathogens promote senescence in the host, and preventing early senescence is a resistance strategy of plants.

  

On the one hand, developmental conditions of the host plant

may determine the outcome of pathogen infection.

  On the other hand, pathogen infection can change the developmental program of the host.

  

Symptoms of senescence often accompany the progression

of disease.

  In other cases, senescence is delayed in response to pathogen infection.

  

The lifestyle of the pathogen plays an important role for the

developmental response of the host

  _{Hemibiotrophs Biotrophs phs} Necrotro Senesce _{Resista Susceptib nce ility} nce

  Ho _st

Figure 1. Relationship between senescence and resistance/susceptibility in

necrotrophic and biotrophic host-pathogen interactions. Biotrophic pathogens and

hemibiotrophs in their biotrophic stage inhibit senescence to increase

susceptibility. The host can control pathogen growth and promote resistance by

activating senescence-like processes. Necrotrophic pathogens and hemibiotrophs

in their necrotrophic stage induce senescence to increase susceptibility. The host

can control pathogen growth and promote resistance by inhibiting senescence-like

processes. Hemibiotrophs switch from a biotrophic to a necrotrophic lifestyle in the

Payers in the control of senescence and pathogen defense:

• Hormon tumbuhan, seperti:

  a. Etilen

  b. Asam Jasmonik

  c. Asam Salisilat

  d. Asam Absisat

  e. Brassinosteroids (BR) sebagai hormon yang mempromosikan senescence Merupakan pemain penting dalam mengendalikan senescence dan pertahanan patogen.

• Hormon tanaman,seperti: a.Sitokinin b.Auksin c.Gibberellin

Hormon Etilen

  Berperan berlawanan pada interaksi dengan patogen necrotropik dan hemibiotropik, yaitu:

   Penuaan dan kematian sel bermanfaat bagi patogen nekrotropik.

  

 Sehingga mensintesa etilen adalah strategi virulensi yang

digunakan patogen nekrotropik dan hemibiotropik.

   Akan tetapi, Etilen berinteraksi secara bersinergi dengan Asam Jasmonik dalam mengaktivasi ketahanan terhadap patogen necrotropik.

Hormon Etilen

  Etilen dapat membantu proses terjadinya senescence

secara tidak langsung, bergantung pada kondisi genetik

dan lingkungan.

Hormon Asam Jasmonik

• Asam Jasmonik memegang peranan penting dalam pengendalian senescence, kematian sel dan ketahanan terhadap patogen nekrotropik.
• Asam Jasmonik dan Asam Absisat membantu ketahanan tanaman dengan serangan serangga dan munculnya luka.

Hormon Asam Salisilat

• Asam Salisilat terutama dikenal sebagai hormon pertahanan, tetapi juga memeiliki peran ganda di dalam mempromosikan perkembangan senescence.
• Asam Salisilat juga dibutuhkan Hypersensitive Response, pada saay terjadinya kematian sel secara lokal. Selama

  terjadinya HR, patogen biotropik ditahan pada tempat terjadi

  infeksi dan mencegah dari penyebaran ke bagian tanaman yang sehat.

Hormon Asam Absisat (ABA)

• ABA mungkin yang paling berperan ganda dalam regulasi senescence dan dalam pengendalian ketahanan terhadap patogen.
• Di satu sisi, ABA termasuk hormon yag memperomosikan senescence.

• Di sisi yang lain, ABA sangat berperan pada ketahanan

  tanaman terhadap patogen biotropik dan nekrotropik.

  Regulatory _{nodes Defence against} Induction of _{senescence ET necrotrophs}

  R _{Induction of senescence JA Defence against necrotrophs} e sis _{Suppression of} ta _{JA/ET- defences SA PTI SAR} n _{Suppression of JA/ET- defences ABA Priming for deposition callose} ce Cell death and _{necrosis ROS Host PTI SAR}

  Pathoge _{impact n}

Figure  7.  A model for the roles of potentially senescence-inducing signaling molecules during necrotrophic host-

pathogen-interactions. Ethylene (ET), jasmonic acid (JA), salicylic acid (SA), abscisic acid (ABA) and reactive oxygen

species (ROS) are usually induced during necrotrophic interactions. If the senescence-promoting effects prevail, host

susceptibility will be increased. If the host succeeds to restrict signaling events to defence-related branches, resistance can

be achieved. Regulatory nodes, such as transcription factors, may act as molecular switches between signaling branches.