| 1. |
- Chen, C., et al.
(författare)
-
Genome-Wide Analysis of Glycine soja Response Regulator GsRR Genes Under Alkali and Salt Stresses
- 2018
-
Ingår i: Frontiers in Plant Science. - : Frontiers Media SA. - 1664-462X. ; 9
-
Tidskriftsartikel (refereegranskat)abstract
- Soil salt-alkalization is a dramatic challenging factor for plant growth. Wild soybean (Glycine soja) exhibits a favorable trait of superior tolerance to salt-alkali stress, and recent discoveries show that response regulator family genes are involved in diverse abiotic stresses. Genomic and transcriptomic analyses of all response regulator genes in wild soybean will provide insight into their function in plant stress response. In this study, we identified and characterized a total of 56 Glycine soja response regulator (GsRR) genes. Phylogenetic analysis suggested that GsRR genes could be classified into five subclasses (A1, A2, B1, B2, and C). We further investigated the chromosome locations, gene duplications and conserved domains of the GsRRs. Furthermore, the clustering analysis of GsRR transcript profiles revealed five different expression patterns under alkali stress. The A1 and A2 subclasses display significantly higher transcriptional levels than the B subclass. In addition, quantitative real-time PCR results verified that the GsRR genes were also significantly influenced by salt stress. Notably, GsRR2a in the A1 subclass showed opposite expression patterns under salt stress comparing with alkali stress. Moreover, overexpression of GsRR2a in Arabidopsis significantly improved the tolerance to alkali stress, but not salt stress. These results suggest the important roles of GsRR genes in response to salt and alkaline stresses, and also provide valuable clues for further functional characterization of GsRR family genes.
|
|
| 2. |
- Fang, W. C., et al.
(författare)
-
Metabolomics in aging research: aging markers from organs
- 2023
-
Ingår i: Frontiers in Cell and Developmental Biology. - 2296-634X. ; 11
-
Tidskriftsartikel (refereegranskat)abstract
- Metabolism plays an important role in regulating aging at several levels, and metabolic reprogramming is the main driving force of aging. Due to the different metabolic needs of different tissues, the change trend of metabolites during aging in different organs and the influence of different levels of metabolites on organ function are also different, which makes the relationship between the change of metabolite level and aging more complex. However, not all of these changes lead to aging. The development of metabonomics research has opened a door for people to understand the overall changes in the metabolic level in the aging process of organisms. The omics-based "aging clock" of organisms has been established at the level of gene, protein and epigenetic modifications, but there is still no systematic summary at the level of metabolism. Here, we reviewed the relevant research published in the last decade on aging and organ metabolomic changes, discussed several metabolites with high repetition rate, and explained their role in vivo, hoping to find a group of metabolites that can be used as metabolic markers of aging. This information should provide valuable information for future diagnosis or clinical intervention of aging and age-related diseases.
|
|
| 3. |
- Jiang, Shan, 1988, et al.
(författare)
-
A comprehensive review of pancreatic cancer and its therapeutic challenges
- 2022
-
Ingår i: Aging. - : Impact Journals, LLC. - 1945-4589. ; 14:18, s. 7635-7649
-
Forskningsöversikt (refereegranskat)abstract
- Pancreatic cancer is a devastating and lethal human malignancy with no curable chemo-treatments available thus far. More than 90% of pancreatic tumors are formed from ductal epithelium as pancreatic ductal adenocarcinoma (PDAC), which often accompany with the expression of mutant K-ras. The incidences of pancreatic cancer are expected to increase rapidly worldwide in the near future, due to environmental pollution, obesity epidemics and etc. The dismal prognosis of this malignancy is contributed to its susceptibility to tumor micro-metastasis from inception and the lack of methods to detect precursor lesions at very early stages of the onset until clinical symptoms occur. In recent years, basic and clinical studies have been making promising progresses for discovering markers to determine the subtypes or stages of this malignancy, which allow effectively implementing personalized therapeutic interventions. The purpose of this review is to discuss the existing knowledge of the molecular mechanisms of pancreatic cancer and the current state of treatment options with the emphasis on targeting therapeutic approaches. The specific focuses are on the molecular mechanisms of the disease, identifications of drug resistance, establishment of immune escaping mechanisms as well as potential of targeting identified pathways in combinations with existing chemo-drugs.
|
|
| 4. |
- Jin, X. J., et al.
(författare)
-
A Genome-Wide Screen in Saccharomyces cerevisiae Reveals a Critical Role for Oxidative Phosphorylation in Cellular Tolerance to Lithium Hexafluorophosphate
- 2021
-
Ingår i: Cells. - : MDPI AG. - 2073-4409. ; 10:4
-
Tidskriftsartikel (refereegranskat)abstract
- Lithium hexafluorophosphate (LiPF6) is one of the leading electrolytes in lithium-ion batteries, and its usage has increased tremendously in the past few years. Little is known, however, about its potential environmental and biological impacts. In order to improve our understanding of the cytotoxicity of LiPF6 and the specific cellular response mechanisms to it, we performed a genome-wide screen using a yeast (Saccharomyces cerevisiae) deletion mutant collection and identified 75 gene deletion mutants that showed LiPF6 sensitivity. Among these, genes associated with mitochondria showed the most enrichment. We also found that LiPF6 is more toxic to yeast than lithium chloride (LiCl) or sodium hexafluorophosphate (NaPF6). Physiological analysis showed that a high concentration of LiPF6 caused mitochondrial damage, reactive oxygen species (ROS) accumulation, and ATP content changes. Compared with the results of previous genome-wide screening for LiCl-sensitive mutants, we found that oxidative phosphorylation-related mutants were specifically hypersensitive to LiPF6. In these deletion mutants, LiPF6 treatment resulted in higher ROS production and reduced ATP levels, suggesting that oxidative phosphorylation-related genes were important for counteracting LiPF6-induced toxicity. Taken together, our results identified genes specifically involved in LiPF6-modulated toxicity, and demonstrated that oxidative stress and ATP imbalance maybe the driving factors in governing LiPF6-induced toxicity.
|
|
| 5. |
- Jin, X. J., et al.
(författare)
-
Functional Roles of Poly(ADP-Ribose) in Stress Granule Formation and Dynamics
- 2021
-
Ingår i: Frontiers in Cell and Developmental Biology. - : Frontiers Media SA. - 2296-634X. ; 9
-
Forskningsöversikt (refereegranskat)abstract
- Stress granules (SGs) are highly dynamic cytoplasmic foci formed in response to stress. The formation of SGs is reported to be regulated by diverse post-translational protein modifications (PTMs). Among them, ADP-ribosylation is of emerging interest due to its recently identified roles in SG organization. In this review, we summarized the latest advances on the roles of poly(ADP-ribose) (PAR) in the regulation of SG formation and dynamics, including its function in modulating nucleocytoplasmic trafficking and SG recruitment of SG components, as well as its effects on protein phase separation behavior. Moreover, the functional role of PAR chain diversity on dynamic of SG composition is also introduced. Potential future developments on investigating global ADP-ribosylation networks, individual roles of different PARPs, and interactions between ADP-ribosylation and other PTMs in SGs are also discussed.
|
|
| 6. |
- Larsson Berglund, Lisa, et al.
(författare)
-
Differential effects of soluble and aggregating polyQ proteins on cytotoxicity and type-1 myosin-dependent endocytosis in yeast
- 2017
-
Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 7
-
Tidskriftsartikel (refereegranskat)abstract
- Huntington's disease develops when the polyglutamine (polyQ) repeat in the Huntingtin (Htt) protein is expanded to over 35 glutamines rendering it aggregation-prone. Here, using Htt exon-1 as a polyQ model protein in a genome-wide screen in yeast, we show that the normal and soluble Htt exon-1 is toxic in cells with defects in type-1 myosin-dependent endocytosis. The toxicity of Htt is linked to physical interactions with type-1 myosins, which occur via the Htt proline-rich region, leading to a reduction in actin patch polarization and clathrin-dependent endocytosis. An expansion of the polyQ stretch from 25 to 103 glutamines, which causes Htt aggregation, alleviated Htt toxicity in cells lacking Myo5 or other components involved in early endocytosis. The data suggest that the proline-rich stretch of Htt interacts with type-1 myosin/clathrin-dependent processes and demonstrate that a reduction in the activity of such processes may result in a positive selection for polyQ expansions.
|
|
| 7. |
- Li, Q., et al.
(författare)
-
Discovery of new strains for furfural degradation using adaptive laboratory evolution in Saccharomyces cerevisiae
- 2023
-
Ingår i: Journal of Hazardous Materials. - 0304-3894. ; 459
-
Tidskriftsartikel (refereegranskat)abstract
- In industrial production, the excessive discharge of furfural can pose harm to soil microorganisms, aquatic an-imals and plants, as well as humans. Therefore, it is crucial to develop efficient and cost-effective methods for degrading furfural in the environment. Currently, the use of Saccharomyces cerevisiae for furfural degradation in water has shown effectiveness, but there is a need to explore improved efficiency and tolerance in S. cerevisiae for this purpose. In this study, we isolated and evolved highly efficient furfural degradation strains, namely YBA_08 and F60C. These strains exhibited remarkable capabilities, degrading 59% and 99% furfural in the YPD medium after 72 h of incubation, significantly higher than the 31% achieved by the model strain S288C. Through analysis of the efficient degradation mechanism in the evolutionary strain F60C, we discovered a 326% increase in the total amount of NADH and NADPH. This increase likely promotes faster furfural degradation through intracel-lular aldehyde reductases. Moreover, the decrease in NADPH content led to a 406% increase in glutathione content at the background level, which protects cells from damage caused by reactive oxygen species. Mutations and differential expression related to cell cycle and cell wall synthesis were observed, enabling cell survival in the presence of furfural and facilitating rapid furfural degradation and growth recovery. Based on these findings, it is speculated that strains YBA_08 and F60C have the potential to contribute to furfural degradation in water and the production of furfuryl alcohol, ethanol, and FDCA in biorefinery processes.
|
|
| 8. |
- Li, X. L., et al.
(författare)
-
Mck1 defines a key S-phase checkpoint effector in response to various degrees of replication threats
- 2019
-
Ingår i: Plos Genetics. - San Francisco : Public Library of Science (PLoS). - 1553-7404 .- 1553-7390. ; 15:8
-
Tidskriftsartikel (refereegranskat)abstract
- The S-phase checkpoint plays an essential role in regulation of the ribonucleotide reductase (RNR) activity to maintain the dNTP pools. How eukaryotic cells respond appropriately to different levels of replication threats remains elusive. Here, we have identified that a conserved GSK-3 kinase Mck1 cooperates with Dun1 in regulating this process. Deleting MCK1 sensitizes dun1 Delta to hydroxyurea (HU) reminiscent of mec1 Delta or rad53 Delta. While Mck1 is downstream of Rad53, it does not participate in the post-translational regulation of RNR as Dun1 does. Mck1 phosphorylates and releases the Crt1 repressor from the promoters of DNA damage-inducible genes as RNR2-4 and HUG1. Hug1, an Rnr2 inhibitor normally silenced, is induced as a counterweight to excessive RNR. When cells suffer a more severe threat, Mck1 inhibits HUG1 transcription. Consistently, only a combined deletion of HUG1 and CRT1, confers a dramatic boost of dNTP levels and the survival of mck1 Delta dun1 Delta or mec1 Delta cells assaulted by a lethal dose of HU. These findings reveal the division-of-labor between Mck1 and Dun1 at the S-phase checkpoint pathway to fine-tune dNTP homeostasis. Author summary The appropriate amount and balance of four dNTPs are crucial for all cells correctly copying and passing on their genetic material generation by generation. Eukaryotes have developed an alert and response system to deal with the disturbance. Here, we uncovered a second-level effector branch. It is activated by the upstream surveillance kinase cascade, which can induce the expression of dNTP-producing enzymes. It can also reduce the inhibitor of these enzymes to further boost their activity according to the degrees of threats. These findings suggest a multi-level response system to guarantee the appropriate dNTP supply, which is essential to maintain genetic stability under various environmental challenges.
|
|
| 9. |
- Lindström, Michelle, et al.
(författare)
-
Lsm7 phase-separated condensates trigger stress granule formation
- 2022
-
Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 13:1
-
Tidskriftsartikel (refereegranskat)abstract
- Stress granules are non-membranous organelles connected to stress responses and age-related disease. Here, the authors identify a conserved yeast protein, Lsm7, that facilitates stress granule formation through dynamic liquid-liquid phase separation condensates upon 2-deoxy-D-glucose-induced stress. Stress granules (SGs) are non-membranous organelles facilitating stress responses and linking the pathology of age-related diseases. In a genome-wide imaging-based phenomic screen, we identify Pab1 co-localizing proteins under 2-deoxy-D-glucose (2-DG) induced stress in Saccharomyces cerevisiae. We find that deletion of one of the Pab1 co-localizing proteins, Lsm7, leads to a significant decrease in SG formation. Under 2-DG stress, Lsm7 rapidly forms foci that assist in SG formation. The Lsm7 foci form via liquid-liquid phase separation, and the intrinsically disordered region and the hydrophobic clusters within the Lsm7 sequence are the internal driving forces in promoting Lsm7 phase separation. The dynamic Lsm7 phase-separated condensates appear to work as seeding scaffolds, promoting Pab1 demixing and subsequent SG initiation, seemingly mediated by RNA interactions. The SG initiation mechanism, via Lsm7 phase separation, identified in this work provides valuable clues for understanding the mechanisms underlying SG formation and SG-associated human diseases.
|
|
| 10. |
|
|
