general stress response
Recently Published Documents


TOTAL DOCUMENTS

228
(FIVE YEARS 55)

H-INDEX

49
(FIVE YEARS 4)

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Antonio D. Moreno ◽  
Cristina González-Fernández ◽  
Elia Tomás-Pejó

AbstractIncreasing yeast robustness against lignocellulosic-derived inhibitors and insoluble solids in bioethanol production is essential for the transition to a bio-based economy. This work evaluates the effect exerted by insoluble solids on yeast tolerance to inhibitory compounds, which is crucial in high gravity processes. Adaptive laboratory evolution (ALE) was applied on a xylose-fermenting Saccharomyces cerevisiae strain to simultaneously increase the tolerance to lignocellulosic inhibitors and insoluble solids. The evolved strain gave rise to a fivefold increase in bioethanol yield in fermentation experiments with high concentration of inhibitors and 10% (w/v) of water insoluble solids. This strain also produced 5% (P > 0.01) more ethanol than the parental in simultaneous saccharification and fermentation of steam-exploded wheat straw, mainly due to an increased xylose consumption. In response to the stress conditions (solids and inhibitors) imposed in ALE, cells induced the expression of genes related to cell wall integrity (SRL1, CWP2, WSC2 and WSC4) and general stress response (e.g., CDC5, DUN1, CTT1, GRE1), simultaneously repressing genes related to protein synthesis and iron transport and homeostasis (e.g., FTR1, ARN1, FRE1), ultimately leading to the improved phenotype. These results contribute towards understanding molecular mechanisms that cells might use to convert lignocellulosic substrates effectively.


Genes ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 53
Author(s):  
Devika Bhave ◽  
Diethard Tautz

Comparative genomic analyses have provided evidence that new genetic functions can emerge out of random nucleotide sequences. Here, we apply a direct experimental approach to study the effects of plasmids harboring random sequence inserts under the control of an inducible promoter. Based on data from previously described experiments dealing with the growth of clones within whole libraries, we extracted specific clones that had shown either negative, neutral or positive effects on relative cell growth. We analyzed these individually with respect to growth characteristics and the impact on the transcriptome. We find that candidate clones for negative peptides lead to growth arrest by eliciting a general stress response. Overexpression of positive clones, on the other hand, does not change the exponential growth rates of hosts, and they show a growth advantage over a neutral clone when tested in direct competition experiments. Transcriptomic changes in positive clones are relatively moderate and specific to each clone. We conclude from our experiments that random sequence peptides are indeed a suitable source for the de novo evolution of genetic functions.


2021 ◽  
Author(s):  
Liping Zeng ◽  
Hao Chen ◽  
Yaqi Wang ◽  
Derrick Hicks ◽  
Haiyan Ke ◽  
...  

Transcriptional regulators of general stress response (GSR) reprogram expression of selected genes to transduce informational signals into cellular events, ultimately manifested in plant's ability to cope with environmental challenges. Identification of the core GSR regulatory proteins will uncover the principal modules and their mode of action in the establishment of adaptive responses. To define the GSR regulatory components, we employed a yeast-one-hybrid assay to identify the protein(s) that binds to the previously established functional GSR motif, coined Rapid Stress Response Element (RSRE). This led to the isolation of ORA47 (octadecanoid-responsive AP2/ERF-domain transcription factor 47), a Methyl jasmonate (MeJA) inducible protein. Subsequently, the ORA47 transcriptional activity was confirmed using RSRE-driven Luciferase (LUC) activity assay performed in the ORA47 loss- and gain-of-function lines introgressed into the 4xRSRE::Luc background. In addition, the prime contribution of CALMODULIN-BINDING TRANSCRIPTIONAL ACTIVATOR3 (CAMTA3) protein in induction of RSRE was reaffirmed by genetic studies. Moreover, exogenous application of MeJA led to enhanced levels of ORA47 and CAMTA3 transcripts, and the induction of RSRE::LUC activity. Metabolic analyses illustrated the reciprocal functional inputs of ORA47 and CAMTA3 in increasing JA levels. Lastly, transient assays identified JASMONATE ZIM-domain1 (JAZ1) as a repressor of RSRE::LUC activity.


2021 ◽  
Author(s):  
Duarte Guerreiro ◽  
M. Graciela Pucciarelli ◽  
Teresa Tiensuu ◽  
Diana Gudynaite ◽  
Aoife Boyd ◽  
...  

The general stress response (GSR) in Listeria monocytogenes plays a critical role in the survival of this pathogen in the host gastrointestinal tract. The GSR is regulated by the alternative sigma factor B (σB), whose role in protection against acid stress is well established. However, the mechanisms leading to its activation by low pH are unknown. Here, we investigated the involvement of the stressosome, a sensory organelle, in transducing low pH signals to induce the GSR. Mild acid shock (15 min at pH 5.0) activated σB and conferred protection against a subsequent lethal pH challenge. A mutant strain where the stressosome subunit RsbR1 was present but its remaining paralogues were genetically inactivated retained the ability to induce σB activity at pH 5.0. The role of stressosome phosphorylation in signal transduction was investigated by mutating the putative phosphorylation sites in the core stressosome proteins RsbR1 (rsbR1 T175A, T209A, T241A) and RsbS (rsbS S56A), or in the active site of the stressosome kinase RsbT (rsbT N49A). The rsbS S56A and rsbT N49A mutations abolished the response to low pH. The rsbR1 T175A variant, retained a near-wild type phenotype. The rsbR1 T209A and rsbR1 T241A mutants displayed constitutive σB activity. Mild acid shock upregulates invasion genes and stimulates epithelial cell invasion, effects that were abolished in mutants with an inactive or overactive stressosome. Overall, the results show that the stressosome is required for acid-induced activation of σB in L. monocytogenes. Furthermore, RsbR1 can function independently of its paralogues and that signal transduction requires RsbT-mediated phosphorylation of RsbS on S56 and RsbR1 on T209. These insights shed light on the mechanisms of signal transduction that activate the GSR in L. monocytogenes in response to acidic environments, and highlight the role this sensory process in the early stages of the infectious cycle.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Michael Bauer ◽  
Manu Shankar-Hari ◽  
Daniel O. Thomas-Rüddel ◽  
Reinhard Wetzker

AbstractIn critically ill patients with sepsis, there is a grave lack of effective treatment options to address the illness-defining inappropriate host response. Currently, treatment is limited to source control and supportive care, albeit with imminent approval of immune modulating drugs for COVID-19-associated lung failure the potential of host-directed strategies appears on the horizon. We suggest expanding the concept of sepsis by incorporating infectious stress within the general stress response of the cell to define sepsis as an illness state characterized by allostatic overload and failing adaptive responses along with biotic (pathogen) and abiotic (e.g., malnutrition) environmental stress factors. This would allow conceptualizing the failing organismic responses to pathogens in sepsis with an ancient response pattern depending on the energy state of cells and organs towards other environmental stressors in general. Hence, the present review aims to decipher the heuristic value of a biological definition of sepsis as a failing stress response. These considerations may motivate a better understanding of the processes underlying “host defense failure” on the organismic, organ, cell and molecular levels.


2021 ◽  
Author(s):  
Devika Bhave ◽  
Diethard Tautz

Comparative genomic analyses have provided evidence that new genetic functions can emerge out of random nucleotide sequences. Here, we apply a direct experimental approach to study the effects of plasmids harbouring random sequence inserts under the control of an inducible promoter. Based on data from previously described experiments dealing with the growth of clones within whole libraries, we extracted specific clones that had shown either negative or positive effects on relative cell growth. We analysed these individually with respect to growth characteristics and impact on the transcriptome. We find that candidate clones for negative peptides lead to growth arrest by eliciting a general stress response. Overexpression of positive clones, on the other hand, does not change the exponential growth rates of hosts, but they show a growth advantage over a neutral candidate clone when tested in direct competition experiments. Transcriptomic changes in positive clones are relatively moderate and specific to each clone. We conclude from our experiments that random sequence peptides are in-deed a suitable source for the de novo evolution of genetic functions.


F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 1162
Author(s):  
Artyom A. Egorov ◽  
Desislava S. Makeeva ◽  
Nadezhda E. Makarova ◽  
Dmitri A. Bykov ◽  
Yanislav S. Hrytseniuk ◽  
...  

In eukaryotes, stalled and collided ribosomes are recognized by several conserved multicomponent systems, which either block protein synthesis in situ and resolve the collision locally, or trigger a general stress response. Yeast ribosome-binding GTPases RBG1 (DRG1 in mammals) and RBG2 (DRG2) form two distinct heterodimers with TMA46 (DFRP1) and GIR2 (DFRP2), respectively, both involved in mRNA translation. Accumulated evidence suggests that the dimers play partially redundant roles in elongation processivity and resolution of ribosome stalling and collision events, as well as in the regulation of GCN1-mediated signaling involved in ribosome-associated quality control (RQC). They also genetically interact with SLH1 (ASCC3) helicase, a key component of RQC trigger (RQT) complex disassembling collided ribosomes. Here, we present RNA-Seq and ribosome profiling (Ribo-Seq) data from S. cerevisiae strains with individual deletions of the TMA46 and GIR2 genes. Raw RNA-Seq and Ribo-Seq data as well as gene-level read counts are available in NCBI Gene Expression Omnibus (GEO) repository under GEO accession GSE185458 and GSE185286.


2021 ◽  
Author(s):  
Gina Esther Merges ◽  
Julia Meier ◽  
Simon Schneider ◽  
Alexander Kruse ◽  
Andreas Christian Fröbius ◽  
...  

One of the key events during spermiogenesis is the hypercondensation of chromatin by substitution of the majority of histones by protamines. In humans and mice, protamine 1 (PRM1/Prm1) and protamine 2 (PRM2/Prm2), are expressed in a species-specific ratio. Using CRISPR-Cas9-mediated gene editing we generated Prm1-deficient mice and demonstrate, that Prm1+/- mice are subfertile while Prm1-/- are infertile. Prm1-deficiency was associated with higher levels of 8-OHdG, an indicator for reactive oxygen mediated DNA-damage. While Prm1+/- males displayed moderate increased levels of 8-OHdG virtually all sperm of Prm1-/- males displayed ROS mediated DNA damage. Consequently, DNA integrity was slightly hampered in Prm1+/-, while DNA was completely fragmented in Prm1-/- animals. Interestingly CMA3 staining which indicates protamine-free DNA revealed, that Prm1+/- sperm displayed high levels (93%), compared to Prm2+/- (29%) and WT (2%) sperm. This is not due to increased histone retention as demonstrated by mass spectrometry (MassSpec) of nuclear proteins in Prm1+/- sperm. Further analysis of the MassSpec data from sperm nuclear proteome revealed, that only one protein (RPL31) is significantly higher abundant in Prm1+/- compared to WT sperm. Comparison of the proteome from Prm1-/- and Prm2-/- to WT suggested, that there are a small number of proteins which differ in abundance. However, their function was not linked mechanistically to primary defects seen in Prm1-/- mice and rather represent a general stress response. Interestingly, using acid urea gels we found that sperm from Prm1+/- and Prm1-/- mice contain a high level of unprocessed, full-length PRM2. Prm2 is transcribed as a precursor protein which, upon binding to DNA is successively processed. Further, the overall ratio of PRM1:PRM2 is skewed from 1:2 in WT to 1:5 in Prm1+/- animals. Our results reveal that Prm1 is required for proper processing of PRM2 to produce the mature PRM2 which, together with Prm1 is able to hypercondense DNA. Hence, the species specific PRM1:PRM2 ratio has to be precisely controlled in order to retain full fertility.


2021 ◽  
Author(s):  
Rubén de Dios ◽  
Eduardo Santero ◽  
Francisca Reyes-Ramírez

Sphingopyxis granuli TFA is a contaminant degrading alphaproteobacterium that responds to adverse conditions by inducing the General Stress Response (GSR), an adaptive response that controls the transcription of a variety of genes to overcome adverse conditions. The GSR triggered by TFA is driven by two extracytoplasmic function σ factors (ECFs), EcfG1 and EcfG2, whose functional differences have been addressed previously, being EcfG2 the main activator. Upstream in this cascade, NepR anti-s factors directly inhibit EcfG activity under non-stress conditions, whereas PhyR response regulators sequester the NepR elements upon stress sensing to relieve EcfG inhibition. These elements, which are essential mediators of the GSR regulation, are duplicated in TFA, being NepR1 and NepR2, and PhyR1 and PhyR2. Here, based on multiple genetic, phenotypical and biochemical evidences including in vitro transcription assays, we have assigned distinct functional features to each of these paralogs and assessed their contribution to the GSR regulation, dictating its timing and the intensity. We show that different stress signals are differentially integrated into the GSR by PhyR1 and PhyR2, therefore producing different levels of GSR activation. We demonstrate in vitro that both NepR1 and NepR2 bind EcfG1 and EcfG2, although NepR1 produces a more stable interaction than NepR2. Conversely, NepR2 interacts with phosphorylated PhyR1 and PhyR2 more efficiently than NepR1. We propose an integrative model where NepR2 would play a dual negative role: it would directly inhibit the s factors upon activation of the GSR and it would modulate the GSR activity indirectly by titrating the PhyR regulators.


Sign in / Sign up

Export Citation Format

Share Document