scholarly journals Cell type specific transcriptional reprogramming of maize leaves during Ustilago maydis induced tumor formation

2019 ◽  
Author(s):  
Mitzi Villajuana-Bonequi ◽  
Alexandra Matei ◽  
Corinna Ernst ◽  
Asis Hallab ◽  
Björn Usadel ◽  
...  

SummaryUstilago maydis is a biotrophic pathogen and well-established genetic model to understand the molecular basis of biotrophic interactions. U. maydis suppresses plant defense and induces tumors on all aerial parts of its host plant maize. In a previous study we found that U. maydis induced leaf tumor formation builds on two major processes: the induction of hypertrophy in the mesophyll and the induction of cell division (hyperplasia) in the bundle sheath. In this study we analyzed the cell-type specific transcriptome of maize leaves 4 days post infection. This analysis allowed identification of key features underlying the hypertrophic and hyperplasic cell identities derived from mesophyll and bundle sheath cells, respectively. We examined the differentially expressed (DE) genes with particular focus on maize cell cycle genes and found that three A-type cyclins, one B-, D- and T-type are upregulated in the hyperplasic tumorous cells, in which the U. maydis effector protein See1 promotes cell division. Additionally, most of the proteins involved in the formation of the pre-replication complex (pre-RC, that assure that each daughter cell receives identic DNA copies), the transcription factors E2Fand DPa as well as several D-type cyclins are deregulated in the hypertrophic cells.

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mitzi Villajuana-Bonequi ◽  
Alexandra Matei ◽  
Corinna Ernst ◽  
Asis Hallab ◽  
Björn Usadel ◽  
...  

2018 ◽  
Vol 217 (4) ◽  
pp. 1681-1695 ◽  
Author(s):  
Alexandra Matei ◽  
Corinna Ernst ◽  
Markus Günl ◽  
Björn Thiele ◽  
Janine Altmüller ◽  
...  

2020 ◽  
Author(s):  
Álvaro Inglés-Prieto ◽  
Nikolas Furthmann ◽  
Samuel Crossman ◽  
Nina Hoyer ◽  
Meike Petersen ◽  
...  

AbstractOptogenetics has been harnessed to shed new mechanistic light on current therapies and to develop future treatment strategies. This has been to date achieved by the correction of electrical signals in neuronal cells and neural circuits that are affected by disease. In contrast, the optogenetic delivery of trophic biochemical signals, which support cell survival and thereby may modify progression of degenerative disorders, has never been demonstrated in an animal disease model. Here, we reengineered the human and Drosophila melanogaster REarranged during Transfection (hRET and dRET) receptors to be activated by light, creating one-component optogenetic tools termed Opto-hRET and Opto-dRET. Upon blue light stimulation, these receptors robustly induced the MAPK/ERK proliferative signaling pathway in cultured cells. In PINK1B9 flies that exhibit loss of PTEN-induced putative kinase 1 (PINK1), a kinase associated with familial Parkinson’s disease (PD), light activation of Opto-dRET suppressed mitochondrial defects, tissue degeneration and behavioral deficits. In human cells with PINK1 loss-of-function, mitochondrial fragmentation was rescued using Opto-dRET via the PI3K/NF-кB pathway. Our results demonstrate that a light-activated receptor can ameliorate disease hallmarks in a genetic model of PD. The optogenetic delivery of trophic signals is cell type-specific and reversible and thus has the potential to overcome limitations of current strategies towards a spatio-temporal regulation of tissue repair.Significance StatementThe death of physiologically important cell populations underlies of a wide range of degenerative disorders, including Parkinson’s disease (PD). Two major strategies to counter cell degeneration, soluble growth factor injection and growth factor gene therapy, can lead to the undesired activation of bystander cells and non-natural permanent signaling responses. Here, we employed optogenetics to deliver cell type-specific pro-survival signals in a genetic model of PD. In Drosophila and human cells exhibiting loss of the PINK1 kinase, akin to autosomal recessive PD, we efficiently suppressed disease phenotypes using a light-activated tyrosine kinase receptor. This work demonstrates a spatio-temporally precise strategy to interfere with degeneration and may open new avenues towards tissue repair in disease models.


2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Chao Zheng ◽  
Yuetong Wang ◽  
Liu Yang ◽  
Shuhua Zhou ◽  
Yijun Gao ◽  
...  

2017 ◽  
Vol 55 (05) ◽  
pp. e28-e56
Author(s):  
S Macheiner ◽  
R Gerner ◽  
A Pfister ◽  
A Moschen ◽  
H Tilg

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