How to define obligatory anaerobiosis? An evolutionary view on the antioxidant response system and the early stages of the evolution of life on Earth

Ślesak, Ireneusz; Kula, Monika; Ślesak, Halina; Miszalski, Zbigniew; Strzałka, Kazimierz

doi:10.1016/j.freeradbiomed.2019.03.004

Cited by 31 publications

(20 citation statements)

References 154 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the oxygenated earth, all of the cellular life forms have evolutionarily established a series of integral cytoprotective systems against various stresses, such that these living organisms are allowed for ecological adaption to the changing environments during development, growth, and other life processes [1]. Hence, it is plausible that there exists at least a set of versatile defense mechanisms (e.g., redox signaling to antioxidant gene regulatory networks) against oxidative stress [1][2][3], which have been brilliantly orchestrated in the prokaryotic to eukaryotic organisms, in order to maintain cell homeostasis and organ integrity under normal physiological and pathophysiological conditions. Amongst them, an evolutionarily conserved family of the cap'n'collar (CNC) basic-region leucine zipper (bZIP) transcription factors is presented across distinct species from marine bacteria to humans [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Nrf1 Is Endowed with a Dominant Tumor-Repressing Effect onto the Wnt/β-Catenin-Dependent and Wnt/β-Catenin-Independent Signaling Networks in the Human Liver Cancer

Chen

Wang

Xiang

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Our previous work revealed that Nrf1α exerts a tumor-repressing effect because its genomic loss (to yield Nrf1α-/-) results in oncogenic activation of Nrf2 and target genes. Interestingly, β-catenin is concurrently activated by loss of Nrf1α in a way similar to β-catenin-driven liver tumor. However, a presumable relationship between Nrf1 and β-catenin is not yet established. Here, we demonstrate that Nrf1 enhanced ubiquitination of β-catenin for targeting proteasomal degradation. Conversely, knockdown of Nrf1 by its short hairpin RNA (shNrf1) caused accumulation of β-catenin so as to translocate the nucleus, allowing activation of a subset of Wnt/β-catenin signaling responsive genes, which leads to the epithelial-mesenchymal transition (EMT) and related cellular processes. Such silencing of Nrf1 resulted in malgrowth of human hepatocellular carcinoma, along with malignant invasion and metastasis to the lung and liver in xenograft model mice. Further transcriptomic sequencing unraveled significant differences in the expression of both Wnt/β-catenin-dependent and Wnt/β-catenin-independent responsive genes implicated in the cell process, shape, and behavior of the shNrf1-expressing tumor. Notably, we identified that β-catenin is not a target gene of Nrf1, but this CNC-bZIP factor contributes to differential or opposing expression of other critical genes, such as CDH1, Wnt5A, Wnt11A, FZD10, LEF1, TCF4, SMAD4, MMP9, PTEN, PI3K, JUN, and p53, each of which depends on the positioning of distinct cis-regulatory sequences (e.g., ARE and/or AP-1 binding sites) in the gene promoter contexts. In addition, altered expression profiles of some Wnt/β-catenin signaling proteins were context dependent, as accompanied by decreased abundances of Nrf1 in the clinic human hepatomas with distinct differentiation. Together, these results corroborate the rationale that Nrf1 acts as a bona fide dominant tumor repressor, by its intrinsic inhibition of Wnt/β-catenin signaling and relevant independent networks in cancer development and malignant progression.

show abstract

Section: Introductionmentioning

confidence: 99%

Nrf1 Is Endowed with a Dominant Tumor-Repressing Effect onto the Wnt/β-Catenin-Dependent and Wnt/β-Catenin-Independent Signaling Networks in the Human Liver Cancer

Chen

Wang

Xiang

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…However, so far such a hypothesis has not been considered in the literature in the context of cereal plant response to the stress caused by the infestation by two pests. Therefore, we undertook to examine parameters of two primeval stress-sensitive metabolic areas, namely the redox balance and photosynthetic efficiency (Ślesak et al 2019 ). The research approach used by us seems to be particularly interesting because CCN attacks roots, while WCM infests leaves, what should cause consequences in the holistic plant response to biotic stressors.…”

Section: Introductionmentioning

confidence: 99%

Reactive oxygen species metabolism and photosynthetic performance in leaves of Hordeum vulgare plants co-infested with Heterodera filipjevi and Aceria tosichella

Labudda

Tokarz

et al. 2020

Plant Cell Rep

View full text Add to dashboard Cite

Key message Defence responses of cyst nematode and/or wheat curl mite infested barley engage the altered reactive oxygen species production, antioxidant machinery, carbon dioxide assimilation and photosynthesis efficiency. Abstract The primary aim of this study was to determine how barley responds to two pests infesting separately or at once; thus barley was inoculated with Heterodera filipjevi (Madzhidov) Stelter (cereal cyst nematode; CCN) and Aceria tosichella Keifer (wheat curl mite; WCM). To verify hypothesis about the involvement of redox metabolism and photosynthesis in barley defence responses, biochemical, photosynthesis efficiency and chlorophyll a fluorescence measurements as well as transmission electron microscopy were implemented. Inoculation with WCM (apart from or with CCN) brought about a significant suppression in the efficiency of electron transport outside photosystem II reaction centres. This limitation was an effect of diminished pool of rapidly reducing plastoquinone and decreased total electron carriers. Infestation with WCM (apart from or with CCN) also significantly restricted the electron transport on the photosystem I acceptor side, therefore produced reactive oxygen species oxidized lipids in cells of WCM and double infested plants and proteins in cells of WCM-infested plants. The level of hydrogen peroxide was significantly decreased in double infested plants because of glutathione–ascorbate cycle involvement. The inhibition of nitrosoglutathione reductase promoted the accumulation of S-nitrosoglutathione increasing antioxidant capacity in cells of double infested plants. Moreover, enhanced arginase activity in WCM-infested plants could stimulate synthesis of polyamines participating in plant antioxidant response. Infestation with WCM (apart from or with CCN) significantly reduced the efficiency of carbon dioxide assimilation by barley leaves, whereas infection only with CCN expanded photosynthesis efficiency. These were accompanied with the ultrastructural changes in chloroplasts during CCN and WCM infestation.

show abstract

“…Since the O2 produced was novel and highly reactive, early cyanobacteria -the first producers of O2would have found exposure to it highly toxic. Environmental pressures likely provided impetus for the evolution of protective enzymes that prevented oxidative damage from reactive oxygen species (ROS) [7][8][9][10] . While it is unclear when defense mechanisms against oxidative damage first evolved, it is reasonable to assume that O2-generating-organisms, such as cyanobacteria, would have co-evolved protective mechanisms as water oxidation proteins evolved.…”

Section: Introductionmentioning

confidence: 99%

Timing the Evolution of Cyanobacterial Antioxidants: Superoxide Dismutases

Boden

Konhauser

Robbins

et al. 2021

Preprint

View full text Add to dashboard Cite

The ancestors of cyanobacteria generated Earth’s first biogenic molecular oxygen but how they dealt with its toxicity remains unconstrained. Here we investigated when superoxide dismutase enzymes (SODs) capable of removing superoxide free radicals evolved. We found phylogenetic evidence that ancestral cyanobacteria used SODs with copper and zinc cofactors (CuZnSOD) during the Archaean. By the Paleoproterozoic, they became genetically capable of using iron, nickel, and manganese as cofactors (FeSOD, NiSOD, and MnSOD respectively). The evolution of NiSOD is particularly intriguing because it has been previously hypothesized that declining seawater Ni concentrations at the end of the Archaean caused a fundamental shift in the marine biosphere away from methanogenesis towards oxygenic photosynthesis. Our novel analyses of enzymes dealing with O2 toxicity now demonstrate that the beneficiaries of this chemical change - marine planktonic cyanobacteria - were able to utilize the remaining Ni from seawater 0.9-0.8 Ga to supplement their existing metabolic capabilities.

show abstract

How to define obligatory anaerobiosis? An evolutionary view on the antioxidant response system and the early stages of the evolution of life on Earth

Cited by 31 publications

References 154 publications

Nrf1 Is Endowed with a Dominant Tumor-Repressing Effect onto the Wnt/β-Catenin-Dependent and Wnt/β-Catenin-Independent Signaling Networks in the Human Liver Cancer

Nrf1 Is Endowed with a Dominant Tumor-Repressing Effect onto the Wnt/β-Catenin-Dependent and Wnt/β-Catenin-Independent Signaling Networks in the Human Liver Cancer

Reactive oxygen species metabolism and photosynthetic performance in leaves of Hordeum vulgare plants co-infested with Heterodera filipjevi and Aceria tosichella

Timing the Evolution of Cyanobacterial Antioxidants: Superoxide Dismutases

Contact Info

Product

Resources

About