Markers for hypersensitive response and senescence show distinct patterns of expression.
Controlled cellular suicide is an important process that can be observed in various organs during plant development. From the generation of proper sexual organs in monoecious plants to the hypersensitive response (HR) that occurs during incompatible pathogen interactions, programmed cell death (PCD) can be readily observed. Although several biochemical and morphological parameters have been described for various types of cell death in plants, the relationships existing between those different types of PCD events remain unclear. In this work, we set out to examine if two early molecular markers of HR cell death (HIN1 and HSR203J) as well as a senescence marker (SAG12) are coordinately induced during these processes. Our result indicates that although there is evidence of some cross-talk between both cell death pathways, spatial and temporal characteristics of activation for these markers during hypersensitive response and senescence are distinct. These observations indicate that these markers are relatively specific for different cell death programs. Interestingly, they also revealed that a senescence-like process seems to be triggered at the periphery of the HR necrotic lesion. This suggests that cells committed to die during the HR might release a signal able to induce senescence in the neighboring cells. This phenomenon could correspond to the establishment of a second barrier against pathogens. Lastly, we used those cell death markers to better characterize cell death induced by copper and we showed that this abiotic induced cell death presents similarities with HR cell death.
Pontier
D
D
Center for Agricultural Molecular Biology, Rutgers, The State University of New Jersey, Cook College, New Brunswick, 08901-0231, USA.
Gan
S
S
Amasino
R M
RM
Roby
D
D
Lam
E
E
D017209:Apoptosis / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D003300:Copper / Q000494:pharmacology; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D017343:Genes, Plant / Q000235:genetics*; D017930:Genes, Reporter / Q000235:genetics; D005819:Genetic Markers / Q000235:genetics; D010935:Plant Diseases; D018515:Plant Leaves / Q000187:drug effects / Q000235:genetics / Q000382:microbiology / Q000502:physiology; D030821:Plants, Genetically Modified; D010947:Plants, Toxic; D011401:Promoter Regions, Genetic / Q000235:genetics; D011549:Pseudomonas / Q000502:physiology; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D014026:Nicotiana / Q000187:drug effects / Q000235:genetics / Q000382:microbiology / Q000502:physiology*; D014027:Tobacco Mosaic Virus / Q000502:physiology*; D015533:Transcriptional Activation / Q000187:drug effects; D019076:Transgenes / Q000235:genetics
D005819:Genetic Markers; D012333:RNA, Messenger; D003300:Copper