Os05g0547850

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Oryza sativa programmed cell death 5 (OsPDCD5) gene is concerned with Programmed cell death (PCD)[1][2][3][4][5].

Annotated Information

Function

  • OsPDCD5 plays an essential role in the regulation of PCD in rice plants. Programmed cell death was accompanied by typical features, including inhibition of developmental growth, a reduction of fresh weight, degradation of total protein content, and fragmentation of genomic DNA[1].
  • Protein degradation and DNA cleavage have determined as tools for the genetic analysis of PCD in transgenic plants, which suggesting that the activation of specific DNase and proteases may be involved in the PCD pathway induced by OsPDCD5 activity. OsPDCD5 activity accelerated the death percentage in transgenic plants and that this was accompanied by the degradation of total protein content[1].
  • Analysis of tissue sections of anthers displays the tapetum cells of the anther wall retard PCD process in transgenic plants under long-day photoperiod. The retarded PCD was also confirmed by DNA fragmentation. In F1 hybrids made from transgenic plants with antisense-OsPDCD5 and japonica rice varieties, lower transcript inhibition could restore fertility, under certain photoperiod and temperatures[2].
  • The male sterility (PGMS) could be used for commercial production of hybrid rice using a two-line breeding system[2]. DNA damage and ROS(Reactive oxygen species) were generally induced by OsPDCD5 overexpression[3], the plant PCD caused by different stress treatments, such as salt and PEG, might have a common regulatory mechanism or exhibit cross-talk[5].
  • The C-terminal of OsCIPK23 might be responsible for the interaction between OsCIPK23 and OsPDCD5 and that the N-terminal of OsCIPK23 was likely to impair this interaction[4]. OsPDCD5 and OsCIPK23 are induced by PEG stress. Overall, OsCIPK23, which interacts with OsPDCD5, was down-regulated under both normal conditions and salt stress treatment in transgenic rice compared to NC rice, which was identical to the response shown by OsPDCD5[5].
  • Antisense-OsPDCD5 affects the transcript levels of numerous salt stressrelated genes, and therefore increases tolerance to salt stress in the transgenic rice[5]. 35s:antisense-OsPDCD5 transgenic rice was shown to increase salt stress tolerance in unique ways by inhibiting PCD pathways and regulating specific groups of stress related genes[5].
  • Overall, OsPDCD5 was induced in NC rice under salt stress. The up-regulated OsPDCD5 induced the expression of some cell death inducers (like Os11g0506800) to initiate PCD. In the meantime, some cell death suppressors (like OsBI-1)were induced to inhibit the occurrence of PCD.When cell death suppressors (like OsBI-1) were not capable of eliminating the effects of OsPDCD5, cells initiated the PCD process. In transgenic rice, antisense-OsPDCD5 repressed the endogenous expression of OsPDCD5. Cell death inducers (like Os11g0506800) and cell death suppressors (like OsBI-1) did not respond, which suggesting that the PCD pathways are inhibited in transgenic rice[5].

Mutation

  • Seven T0 transgenic rice plants[2]:
    • They were selected based on PCR detection, transgenic rice showed more sensitive to photoperiod changes compared with the control(Zhonghua 11).
    • The level of OsPDCD5 mRNA in transgenic tissues was less than that in Zhonghua 11, especially in apical meristem, young leaves and young panicles.
  • T3 transgenic plants[2]:

OsPDCD5 mRNA was decreased in transgenic rice, consistent with the extent of pollen abortion observed.

  • Transgenic plants and control 9311[3]
  • T3 transgenic rice[5]:
    • Endogenous OsPDCD5 was inhibited by antisense-OsPDCD5 in transgenic rice throughout the salt stress treatment period.
    • Expression analyses identified 38 genes that showed a more than two-fold change in transcript level in transgenic plants compared to that in NC plants.
    • In both transgenic and NC rice, OsCIPK23 was increased under salt stress treatment. The increment was considerably larger in NC rice than in transgenic rice throughout the treatment period, which was also similar to the expression profile of OsPDCD5.

Expression

  • The antisense-OsPDCD5 expressed in various tissues of transgenic rice, such as leaf primordium surrounding the shoot apical meristem, young leaves and young anthers, including pollen and anther wall cells[2].
  • Ectopic OsPDCD5 overexpression efficaciously induced cell death with multiple PCD features, such as DNA fragmentation, ROS formation, and mitochondrial dysfunction)[3].
  • In both the ZH and NT group seedlings, ectopic OsPDCD5 expression efficaciously induced PCD in three-leaf stage and older seedlings but did not induce any visible morphological phenotypes in two-leaf stage and younger seedlings[3].
  • Its overexpression can induce PCD in transgenic rice. immunoblotting analysis revealed that the OsPDCD5 protein was widely expressed in the tassel, leaf, leaf sheath, and different parts of the stem but not in the anther. RT-PCR analysis showed that OsPDCD5 was related to the senescence of leaf and root tissues as well as the development of stem tissues. Furthermore, OsPDCD5 was up-regulated by UV-B irradiation. Calcineurin B-like interacting protein kinase 23 (OsCIPK23), which is involved in the calcineurin B-like proteins (CLBs)/CBL-interacting protein kinases (CIPKs) signaling network, was identified as interacting with OsPDCD5 by yeast two-hybrid screening and subsequently confirmed by pull-down assay in vitro[4].
  • OsPDCD5 expression was enhanced in response to various abiotic stresses such as UV-B irradiation, low temperature, and salt treatment[4][5]. OsPDCD5 expression was induced by developmental and environmental cues and identified an interaction between OsPDCD5 and OsCIPK23[4].
  • OsPDCD5 increased salt stress tolerance in unique ways by inhibiting PCD pathways and regulating specific groups of stress-related genes. Realtime quantitative PCR analysis showed that PCD pathways were inhibited under both normal conditions and salt stress in transgenic rice[5].

Localization

OsPDCD5 was predominantly localized to the tapetal layer[3].

Evolution

  • The deduced amino acid sequence of OsPDCD5 was conserved in several different species, including Arabidopsis thaliana (Accession No. NP564336), Homo sapiens (Accession No. AAP36696) and mice (Accession No. NP062720). Alignment of the amino acid sequences of rice programmed cell death 5 gene (OsPDCD5) of rice (Oryza sativa)(Os) with putative apoptosis-related protein 19 of Arabidopsis (At; 64% identity), Homo sapiens (Hs; 39% identity) and Mouse (M; 39% identity).[1].
  • OsPDCD5, is an ortholog to mammalian programmed cell death 5(PDCD5) gene, which involved in programmed cell death (PCD)regulation and highly conserved over time[2][3].

Knowledge Extension

Programmed cell death (PCD), or apoptosis, is an evolutionarily conserved form of cell suicide that requires active gene expression[6] and occurs in multicellular organisms throughout development, as well as in response to biotic and abiotic stresses. In plants, PCD plays a critical role in a number of developmental events, such as cell death during xylogenesis, aerenchyma formation, several plant reproductive processes, leaf and petal senescence, and endosperm development[7][8]. Furthermore, cell death in response to pathogen attack, as well as in response to a variety of abiotic factors, such as ozone and ultraviolet (UV) radiation, also falls within the definition of PCD[9]

Labs working on this gene

  • State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, 220 Handan Road, Shanghai 200433, China

References

  1. ↑ 1.0 1.1 1.2 1.3 ATTIA K, LI K G, WEI C, et al. Overexpression of the OsPDCD5 gene induces programmed cell death in rice[J]. Journal of Integrative Plant Biology, 2005, 47(9): 1115-1122.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Wang Y, Zha X, Zhang S, et al. Down-regulation of the< i> OsPDCD5</i> gene induced photoperiod-sensitive male sterility in rice[J]. Plant science, 2010, 178(2): 221-228.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Sun F, Qi W, Qian X, et al. Investigating the role of OsPDCD5, a homolog of the mammalian PDCD5, in programmed cell death by inducible expression in rice[J]. Plant Molecular Biology Reporter, 2012, 30(1): 87-98.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 Su W, Wu J, Wei C, et al. Interaction between programmed cell death 5 and calcineurin B-like interacting protein kinase 23 in< i> Oryza sativa</i>[J]. Plant science, 2006, 170(6): 1150-1155.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 Yang M, Sun F, Wang S, et al. Down-regulation of OsPDCD5, a homolog of the mammalian PDCD5, increases rice tolerance to salt stress[J]. Molecular Breeding, 2013, 31(2): 333-346.
  6. ↑ Lam E, Kato N, Lawton M. Programmed cell death, mitochondria and the plant hypersensitive response[J]. Nature, 2001, 411(6839): 848-853.
  7. ↑ Quirino B F, Noh Y S, Himelblau E, et al. Molecular aspects of leaf senescence[J]. Trends in plant science, 2000, 5(7): 278-282.
  8. ↑ Gunawardena A H, Greenwood J S, Dengler N G. Programmed cell death remodels lace plant leaf shape during development[J]. The Plant Cell Online, 2004, 16(1): 60-73.
  9. ↑ Woltering E J. Death proteases come alive[J]. Trends in plant science, 2004, 9(10): 469-472.

Structured Information

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