scholarly journals Interplay of the RNA Exosome Complex and RNA-Binding Protein Ssd1 in Maintaining Cell Wall Stability in Yeast

Author(s):  
Ana Novačić ◽  
Nada Šupljika ◽  
Nikša Bekavac ◽  
Bojan Žunar ◽  
Igor Stuparević

Stressful conditions such as high temperatures can compromise cellular integrity and cause bursting. In microorganisms surrounded by a cell wall, such as yeast, the cell wall is the primary shield that protects cells from environmental stress.

Genetics ◽  
2010 ◽  
Vol 185 (2) ◽  
pp. 513-522 ◽  
Author(s):  
Joshua J. Wolf ◽  
Robin D. Dowell ◽  
Shaun Mahony ◽  
Michal Rabani ◽  
David K. Gifford ◽  
...  

2011 ◽  
Vol 10 (10) ◽  
pp. 1340-1347 ◽  
Author(s):  
Wataru Ito ◽  
Xia Li ◽  
Kaoru Irie ◽  
Tomoaki Mizuno ◽  
Kenji Irie

ABSTRACT The Saccharomyces cerevisiae RNA-binding protein Khd1/Hek2 associates with hundreds of potential mRNA targets preferentially, including the mRNAs encoding proteins localized to the cell wall and plasma membrane. We have previously revealed that Khd1 positively regulates expression of MTL1 mRNA encoding a membrane sensor in the cell wall integrity (CWI) pathway. However, a khd1 Δ mutation has no detectable phenotype on cell wall synthesis. Here we show that the khd1 Δ mutation causes a severe cell lysis when combined with the deletion of the CCR4 gene encoding a cytoplasmic deadenylase. We identified the ROM2 mRNA, encoding a guanine nucleotide exchange factor (GEF) for Rho1, as a target for Khd1 and Ccr4. The ROM2 mRNA level was decreased in the khd1 Δ ccr4 Δ mutant, and ROM2 overexpression suppressed the cell lysis of the khd1 Δ ccr4 Δ mutant. We also found that Ccr4 negatively regulates expression of the LRG1 mRNA encoding a GTPase-activating protein (GAP) for Rho1. The LRG1 mRNA level was increased in the ccr4 Δ and khd1 Δ ccr4 Δ mutants, and deletion of LRG1 suppressed the cell lysis of the khd1 Δ ccr4 Δ mutant. Our results presented here suggest that Khd1 and Ccr4 modulate a signal from Rho1 in the CWI pathway by regulating the expression of RhoGEF and RhoGAP.


2018 ◽  
Vol 23 (12) ◽  
pp. 988-997 ◽  
Author(s):  
Nguyen Thi Minh Viet ◽  
Duong Long Duy ◽  
Kazuhiro Saito ◽  
Kaoru Irie ◽  
Yasuyuki Suda ◽  
...  

2019 ◽  
Vol 294 (26) ◽  
pp. 10349-10364 ◽  
Author(s):  
Karina B. Sabalette ◽  
María Albertina Romaniuk ◽  
Griselda Noé ◽  
Alejandro Cassola ◽  
Vanina A. Campo ◽  
...  

Oncogenesis ◽  
2019 ◽  
Vol 8 (12) ◽  
Author(s):  
Xiaona Zhang ◽  
Yanchun Zhou ◽  
Shaoying Chen ◽  
Wei Li ◽  
Weibing Chen ◽  
...  

AbstractLong noncoding RNA (lncRNA) represents a class of endogenous RNAs that regulate gene expression in eukaryotes. To date, the function and underlying mechanism of the majority of mammalian lncRNAs remain unknown. Here, we report that MACC1-AS1, a cognate antisense lncRNA of the sixth intron of the MACC1 gene, functions as a cell growth modulator and enhances breast tumor progress. RNA pulldown and luciferase assays showed that MACC1-AS1 contained binding sites for multiple miRNAs, including well-known tumor suppressors miR-384 and miR-145-3p that repress the expression of pleiotrophin (PTN) and c-Myc mRNAs. Binding of miR-384 and miR-145-3p miRNAs to MACC1-AS1 alters the cell growth phenotype through increased expression of PTN and c-Myc mRNAs. MACC1-AS1 also competitively interacted with PTBP1, an RNA-binding protein, via a conserved pyrimidine rich motif within this lncRNA. Binding of PTBP1to MACC1-AS1 not only stabilized MACC1-AS1 and enhanced the sponge effect of MACC1-AS1 on miRNAs, but also decreased PTBP1 availability for binding to target mRNAs. Our results define a new dimension into how a lncRNA is able to regulate cell growth by sponging multiple miRNAs and an RNA-binding protein.


1994 ◽  
Vol 26 (3) ◽  
pp. 833-849 ◽  
Author(s):  
Heimo Breiteneder ◽  
Christine B. Michalowski ◽  
Hans J. Bohnert

Author(s):  
Arnika Przybylska ◽  
Maciej Spychalski

Abstract Background Meloidogyne arenaria is an economically important root-knot nematode (RKN) species whose hosts include maize (Zea mays). The plant response to RKN infection activates many cellular mechanisms, among others, changes in the expression level of genes encoding transcription and elongation factors as well as proteins related to cell wall organization. Methods and results This study is aimed at characterization of expression of selected transcription and elongation factors encoding the genes WRKY53, EF1a, and EF1b as well as the ones encoding two proteins associated with cell wall functioning (glycine-rich RNA-binding protein, GRP and polygalacturonase, PG) during the maize response to M. arenaria infection. The changes in the relative level of expression of genes encoding these proteins were assessed using the reverse transcription-quantitative real-time PCR. The material studied were leaves and root samples collected from four maize varieties showing different susceptibilities toward M. arenaria infection, harvested at three different time points. Significant changes in the expression level of GRP between susceptible and tolerant varieties were observed. Conclusions Results obtained in the study suggest pronounced involvement of glycine-rich RNA-binding protein and EF1b in the maize response and resistance to RKN.


2020 ◽  
Author(s):  
Lin-Chun Chang ◽  
Yu-Chieh Wu ◽  
Yu-Yun Chang ◽  
Fang-Jen Lee

AbstractThe yeast cell wall integrity (CWI) MAPK pathway is a signaling cascade function in maintaining cell wall integrity under stressful environmental conditions. Recently, the activity and signaling of Slt2p (Mpk1p) MAP kinase has been shown to control assembly of the processing body (P-body) upon cell wall stresses, implicating its posttranscriptional role in decay of cell wall mRNAs. However, how Slt2p MAP kinase directly regulates the stability of cell wall transcripts during cell wall stress remains unclear. Here, we reported that the RNA-binding protein Rbp1p (Ngr1p) is a downstream effector and target of Slt2p MAP kinase during activation of the cell wall stress signaling cascade. In addition to the well-defined target mitochondrial porin mRNA, we found that Rbp1p also negatively regulates the stability of a subset of Slt2p-regulated cell wall transcripts. Deletion of RBP1 increases the level of cell wall transcripts and partially suppresses the hypersensitivity of the slt2Δ deletion strain to cell wall damage. Slt2p is necessary for cell wall stress-induced stabilization of cell wall transcripts. Deletion of RBP1 compromises the destabilization of cell wall transcripts in slt2Δ mutants under cell wall stress. Notably, C-terminal deleted Slt2p impairs its function in promoting turnover of the Rbp1p protein and fails to stabilize cell wall transcripts, although it can complement the growth defect of the slt2Δ strain upon cell wall stress. Altogether, our results demonstrate that MAP kinase Slt2p attenuates CWI mRNA decay in response to cell wall damage by downregulating the activity of the RNA-binding protein Rbp1p.


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