Speaker
Description
Endoplasmic Reticulum (ER) is a vital part for functional protein synthesis in eukaryotic cells. ER stress is caused by over-accumulation of unfolded or misfolded proteins, which are massively produced in dysfunctional protein synthesis, in the ER lumen. For a plant cell, ER stress can be induced by various environment factors, such as abiotic stress, saline stress and heat stress. At the same time, unfolded protein response (UPR) is an essential defensive mechanism in plant cells to alleviate ER stress.
Unlike the UPR in mammalian cells, only two pathways have been identified: IRE1$\alpha/\beta$ and bZIP28 pathway. Both IRE1$\alpha/\beta$ and bZIP28 are ER stress sensors on the ER membrane. IRE1$\alpha/\beta$ is activated when sensing the accumulation of unfolded protein in the ER lumen and then catalyse the splicing of bZIP60 mRNA. Spliced bZIP60 mRNA will finally be translated to bZIP60 transcription factor. For bZIP28, when activated, it will dissociate from the ER membrane and then be cleaved by protease at Golgi before turning to a transcription factor. The transcription factor bZIP60 and bZIP28 can then initiate the transcription of a group of UPR genes. A molecular chaperone gene BiP is one of the typical UPR genes and BiP protein can help alleviate ER stress by refolding the badly folded proteins in the ER lumen.
In recent researches, ER stress was found to be linked with plant programmed cell death (PCD). Under prolonged ER stress, plant cells would finally go to PCD by showing caspase-like activity in the cell. Additionally, more evidences were presented to link ER stress and plant PCD, one important transcription factor, NAC089, was found not only to be involved in UPR signalling (controlled by both bZIP60 and bZIP28), but also could promote PCD for the plant cells. So the role of NAC089 in plant cells could potentially be the deciding factor of the cell fate. We used both experimental and computational method to further understand the UPR in plant cells and the role of NAC089 plays under ER stress. We first present the functions of cathepsin B and proteasome under ER stress, which are more evidences about the link between ER stress and plant PCD. Next, we present a novel mathematical model about the UPR signalling, including NAC089 in plant cell with ordinary differential equations (ODEs). We also use both algebraic and numerical method to analyse our UPR model.
To have an insight of the survival and PCD for Arabidopsis, we present our data using different experimental systems. We also show the designing of an original `Time-Dose' matrix method for plant seedling system, which shows clear seedling phenotype difference using different ER stress conditions. Finally, we use our UPR model to compare the transcript changes with experimental data and find that our UPR model still needs improvement although it makes some promising predictions.
