Programmed cell death in plant disease: The purpose and promise of cellular suicide

被引:200
作者
Gilchrist, DG [1 ]
机构
[1] Univ Calif Davis, Dept Plant Pathol, Davis, CA 95616 USA
[2] Univ Calif Davis, NSF Ctr Engn Plants Resistance Pathogens, CEPRAP, Davis, CA 95616 USA
关键词
apoptosis; lesion mimics; hypersensitive reaction; ceramide; cell cycle;
D O I
10.1146/annurev.phyto.36.1.393
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The interaction of pathogens with plants leads to a disruption in cellular homeostasis, often leading to cell death, in both compatible and incompatible relationships. The mechanistic basis of this cellular disruption and consequent death is complex and poorly characterized, but it is established that host responses to pathogens are dependent on gene expression, involve signal transduction, and require energy. Recent data suggest that in animals, a genetically regulated, signal transduction-dependent programmed cell death process, commonly referred to as apoptosis, is conserved over a wide range of phyla. The basic function of apoptosis is to direct the selective elimination of certain cells during development, but it also is a master template that is involved in host responses to many pathogens. Programmed cell death in plants, while widely observed, has not been studied extensively at either the biochemical or genetic level. Current data suggest that activation or suppression of programmed cell death may underlie diseases in plants as it does in animals. This review describes some of the fundamental characteristics of apoptosis in animals and points to a number of connections to programmed cell death in plants that may lead to both a better understanding of disease processes and novel strategies for engineering disease resistance in plants.
引用
收藏
页码:393 / 414
页数:22
相关论文
共 125 条
[1]   FUMONISIN-INDUCED AND AAL-TOXIN-INDUCED DISRUPTION OF SPHINGOLIPID METABOLISM WITH ACCUMULATION OF FREE SPHINGOID BASES [J].
ABBAS, HK ;
TANAKA, T ;
DUKE, SO ;
PORTER, JK ;
WRAY, EM ;
HODGES, L ;
SESSIONS, AE ;
WANG, E ;
MERRILL, AH ;
RILEY, RT .
PLANT PHYSIOLOGY, 1994, 106 (03) :1085-1093
[2]   APOPTOSIS - REGULATION AND RELEVANCE TO TOXICOLOGY [J].
ALISON, MR ;
SARRAF, CE .
HUMAN & EXPERIMENTAL TOXICOLOGY, 1995, 14 (03) :234-247
[3]   The origin of programmed cell death [J].
Ameisen, JC .
SCIENCE, 1996, 272 (5266) :1278-1279
[4]   PERTURBATION OF THE UBIQUITIN SYSTEM CAUSES LEAF CURLING, VASCULAR TISSUE ALTERATIONS AND NECROTIC LESIONS IN A HIGHER-PLANT [J].
BACHMAIR, A ;
BECKER, F ;
MASTERSON, RV ;
SCHELL, J .
EMBO JOURNAL, 1990, 9 (13) :4543-4549
[5]   ACTIVE OXYGEN IN PLANT PATHOGENESIS [J].
BAKER, CJ ;
ORLANDI, EW .
ANNUAL REVIEW OF PHYTOPATHOLOGY, 1995, 33 :299-321
[6]   Apoptosis - The cell's silent exit [J].
Bar, PR .
LIFE SCIENCES, 1996, 59 (5-6) :369-378
[7]   Programmed cell death during plant growth and development [J].
Beers, EP .
CELL DEATH AND DIFFERENTIATION, 1997, 4 (08) :649-661
[8]   The molecular biology of leaf senescence [J].
BuchananWollaston, V .
JOURNAL OF EXPERIMENTAL BOTANY, 1997, 48 (307) :181-199
[9]   DETERMINATION OF THE LENGTH OF THE HISTOLOGICAL STAGES OF APOPTOSIS IN NORMAL LIVER AND IN ALTERED HEPATIC FOCI OF RATS [J].
BURSCH, W ;
PAFFE, S ;
PUTZ, B ;
BARTHEL, G ;
SCHULTEHERMANN, R .
CARCINOGENESIS, 1990, 11 (05) :847-853
[10]   The barley mlo gene: A novel control element of plant pathogen resistance [J].
Buschges, R ;
Hollricher, K ;
Panstruga, R ;
Simons, G ;
Wolter, M ;
Frijters, A ;
vanDaelen, R ;
vanderLee, T ;
Diergaarde, P ;
Groenendijk, J ;
Topsch, S ;
Vos, P ;
Salamini, F ;
Schulze-Lefert, P .
CELL, 1997, 88 (05) :695-705