scholarly journals Beyond Ethylene: New Insights Regarding the Role of AOX in the Respiratory Climacteric

Author(s):  
Seanna Hewitt ◽  
Amit Dhingra

Climacteric fruits are characterized by a dramatic increase in autocatalytic ethylene production, which is accompanied by a spike in respiration, at the onset of ripening. The change in the mode of ethylene production from autoinhibitory to auto-stimulatory is known as the system 1 (S1) to system 2 (S2) transition. Existing physiological models explain the basic and overarching genetic, hormonal, and transcriptional regulatory mechanisms governing the S1 to S2 transition of climacteric fruit. However, the links between ethylene and respiration, the two main factors that characterize the respiratory climacteric, have been largely understudied at the molecular level. Results of recent studies indicate that the AOX respiratory pathway may play an important role in mediating cross talk between ethylene response, carbon metabolism, ATP production, and ROS signaling during climacteric ripening. New genomic, metabolic, and epigenetic information sheds light on the interconnectedness of ripening-associated metabolic pathways, necessitating expanding the current, ethylene-centric physiological models. Understanding points at which ripening responses can be manipulated may reveal key, speciesand cultivar-specific targets for regulation of ripening enabling superior strategies for reducing postharvest wastage.

2019 ◽  
Vol 6 (2) ◽  
pp. 15 ◽  
Author(s):  
Angel Dueñas ◽  
Almudena Expósito ◽  
Amelia Aranega ◽  
Diego Franco

Cardiovascular development is a complex developmental process starting with the formation of an early straight heart tube, followed by a rightward looping and the configuration of atrial and ventricular chambers. The subsequent step allows the separation of these cardiac chambers leading to the formation of a four-chambered organ. Impairment in any of these developmental processes invariably leads to cardiac defects. Importantly, our understanding of the developmental defects causing cardiac congenital heart diseases has largely increased over the last decades. The advent of the molecular era allowed to bridge morphogenetic with genetic defects and therefore our current understanding of the transcriptional regulation of cardiac morphogenesis has enormously increased. Moreover, the impact of environmental agents to genetic cascades has been demonstrated as well as of novel genomic mechanisms modulating gene regulation such as post-transcriptional regulatory mechanisms. Among post-transcriptional regulatory mechanisms, non-coding RNAs, including therein microRNAs and lncRNAs, are emerging to play pivotal roles. In this review, we summarize current knowledge on the functional role of non-coding RNAs in distinct congenital heart diseases, with particular emphasis on microRNAs and long non-coding RNAs.


Author(s):  
John Mason

Everyone gets stuck sometimes, and it can sometimes be frustrating, even debilitating rather than stimulating. However, being stuck is an honourable and useful state because that is when it is possible to learn about mathematics, about mathematical thinking, and about oneself. This applies especially to teachers, because the best way to sensitise yourself to learners’ struggles is to experience parallel struggles yourself. People are usually eager to get unstuck, to locate and enact some hopefully helpful action, without attending to how they got stuck in the first place, nor how the fresh action arose. I propose to dwell in the states of becoming and being stuck, and to use this as a springboard to examine and amplify the notion of ‘having some possibility come-to-mind’ as a means to get unstuck. This will include an expansion of the notions of system 1 and system 2 (automatic-habitual reaction and considered response) from dual systems theory, so as to take account of the full human psyche and development of the role of reflection. My method will be as phenomenological as possible, drawing on specific accounts from my own experience, but hoping to resonate with the experience of readers.


Author(s):  
Randy Moore

Previous work has indicated that the graft incompatihility between Sedrmi telephoides and Solanum pennellil involves cell necrosis that results In a thick layer of collapsed cells at the graft Interface. This necrotic layer insulates the stock from the scion, which results in abscission of the Sedum scion after 4-6 weeks due to desiccation and starvation. Thus, cell autolysis (which is restricted to Sedum) characterizes the Incompatibility response in this system (1). In order to elucidate the events that lead to cell autolysis, and thus better understand the cellular site and mode of action of cellular incompatibility, the appearance and fate of the hydrolytlc enzyme acid phosphatase (AP) was followed in both the compatible Sedum autograft and the incompatible Sedum/Solanum heterograft. Acid phosphatase was localized by a modified Gomori-type reaction; positive (i.e., including NaF inhibitor) and negative (lacking substrate) controls showed no enzymatic precipitate. Following an initial association with the endoplasmic reticulum (ER) and dictyosomes at 6-10 hours after grafting, AP activity in the compatible Sedum autograft is associated primarily with the plasmalemma (Fig. 1). By 18-24 hours after grafting, the AP activity is restricted to the tono-plast and vacuole (Fig. 2). This strict compartmentation and absence of enzyme from the cytosol is maintained throughout the development of the compatible graft. While AP activity in the incompatible Sedum/Solanum heterograft is Initially similar to the compatible Sedum autograft (i.e., initially found on the ER and dictyosomes), there is a marked difference in enzyme localization in the two graft partners as the incompatibility response develops. As in the compatible autograft, Solanum cells at the graft interface show an Increase in AP activity that Is restricted to the vacuole and tonoplast, with little or no enzyme activity in the cytosol (Fig. 3). In comparable Sedum cells, however, there is a dramatic Increase In AP activity in the cytosol (Fig. h); this cytosollc AP activity is associated with thin fibril-like structures (Fig. 5) measuring approximately 60 A in diameter. This high cytoplasmic AP activity In Sedum cells results in cell autolysis, death, and eventual cell collapse to form the characteristic necrotic layer separating the two graft partners.


2004 ◽  
Vol 40 ◽  
pp. 41-58 ◽  
Author(s):  
William B Pratt ◽  
Mario D Galigniana ◽  
Yoshihiro Morishima ◽  
Patrick J M Murphy

Unliganded steroid receptors are assembled into heterocomplexes with heat-shock protein (hsp) 90 by a multiprotein chaperone machinery. In addition to binding the receptors at the chaperone site, hsp90 binds cofactors at other sites that are part of the assembly machinery, as well as immunophilins that connect the assembled receptor-hsp90 heterocomplexes to a protein trafficking pathway. The hsp90-/hsp70-based chaperone machinery interacts with the unliganded glucocorticoid receptor to open the steroid-binding cleft to access by a steroid, and the machinery interacts in very dynamic fashion with the liganded, transformed receptor to facilitate its translocation along microtubular highways to the nucleus. In the nucleus, the chaperone machinery interacts with the receptor in transcriptional regulatory complexes after hormone dissociation to release the receptor and terminate transcriptional activation. By forming heterocomplexes with hsp90, the chaperone machinery stabilizes the receptor to degradation by the ubiquitin-proteasome pathway of proteolysis.


Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 966
Author(s):  
Florencia Cascardo ◽  
Nicolás Anselmino ◽  
Alejandra Páez ◽  
Estefanía Labanca ◽  
Pablo Sanchis ◽  
...  

Prostate cancer (PCa) is the second most diagnosed malignancy and the fifth leading cause of cancer associated death in men worldwide. Dysregulation of cellular energetics has become a hallmark of cancer, evidenced by numerous connections between signaling pathways that include oncoproteins and key metabolic enzymes. We previously showed that heme oxygenase 1 (HO-1), a cellular homeostatic regulator counteracting oxidative and inflammatory damage, exhibits anti-tumoral activity in PCa cells, inhibiting cell proliferation, migration, tumor growth and angiogenesis. The aim of this study was to assess the role of HO-1 on the metabolic signature of PCa. After HO-1 pharmacological induction with hemin, PC3 and C4-2B cells exhibited a significantly impaired cellular metabolic rate, reflected by glucose uptake, ATP production, lactate dehydrogenase (LDH) activity and extracellular lactate levels. Further, we undertook a bioinformatics approach to assess the clinical significance of LDHA, LDHB and HMOX1 in PCa, identifying that high LDHA or low LDHB expression was associated with reduced relapse free survival (RFS). Interestingly, the shortest RFS was observed for PCa patients with low HMOX1 and high LDHA, while an improved prognosis was observed for those with high HMOX1 and LDHB. Thus, HO-1 induction causes a shift in the cellular metabolic profile of PCa, leading to a less aggressive phenotype of the disease.


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1720
Author(s):  
Kuo-Chieh Liao ◽  
Mariano A. Garcia-Blanco

The importance of transcriptional regulation of host genes in innate immunity against viral infection has been widely recognized. More recently, post-transcriptional regulatory mechanisms have gained appreciation as an additional and important layer of regulation to fine-tune host immune responses. Here, we review the functional significance of alternative splicing in innate immune responses to viral infection. We describe how several central components of the Type I and III interferon pathways encode spliced isoforms to regulate IFN activation and function. Additionally, the functional roles of splicing factors and modulators in antiviral immunity are discussed. Lastly, we discuss how cell death pathways are regulated by alternative splicing as well as the potential role of this regulation on host immunity and viral infection. Altogether, these studies highlight the importance of RNA splicing in regulating host–virus interactions and suggest a role in downregulating antiviral innate immunity; this may be critical to prevent pathological inflammation.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lei Chen ◽  
Shirley Luo ◽  
Abigail Dupre ◽  
Roshan P. Vasoya ◽  
Aditya Parthasarathy ◽  
...  

AbstractThe brush border is comprised of microvilli surface protrusions on the apical surface of epithelia. This specialized structure greatly increases absorptive surface area and plays crucial roles in human health. However, transcriptional regulatory networks controlling brush border genes are not fully understood. Here, we identify that hepatocyte nuclear factor 4 (HNF4) transcription factor is a conserved and important regulator of brush border gene program in multiple organs, such as intestine, kidney and yolk sac. Compromised brush border gene signatures and impaired transport were observed in these tissues upon HNF4 loss. By ChIP-seq, we find HNF4 binds and activates brush border genes in the intestine and kidney. H3K4me3 HiChIP-seq identifies that HNF4 loss results in impaired chromatin looping between enhancers and promoters at gene loci of brush border genes, and instead enhanced chromatin looping at gene loci of stress fiber genes in the intestine. This study provides comprehensive transcriptional regulatory mechanisms and a functional demonstration of a critical role for HNF4 in brush border gene regulation across multiple murine epithelial tissues.


Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 264
Author(s):  
Kathryn E. Ritz ◽  
Bradley J. Heins ◽  
Roger D. Moon ◽  
Craig C. Sheaffer ◽  
Sharon L. Weyers

Organic dairy cows were used to evaluate the effect of two organic pasture production systems (temperate grass species and warm-season annual grasses and cool-season annuals compared with temperate grasses only) across two grazing seasons (May to October of 2014 and 2015) on milk production, milk components (fat, protein, milk urea nitrogen (MUN), somatic cell score (SCS)), body weight, body condition score (BCS), and activity and rumination (min/day). Cows were assigned to two pasture systems across the grazing season at an organic research dairy in Morris, Minnesota. Pasture System 1 was cool-season perennials (CSP) and Pasture System 2 was a combination of System 1 and warm-season grasses and cool-season annuals. System 1 and System 2 cows had similar milk production (14.7 and 14.8 kg d−1), fat percentage (3.92% vs. 3.80%), protein percentage (3.21% vs. 3.17%), MUN (12.5 and 11.5 mg dL−1), and SCS (4.05 and 4.07), respectively. Cows in System 1 had greater daily rumination (530 min/day) compared to cows in System 2 (470 min/day). In summary, warm-season annual grasses may be incorporated into grazing systems for pastured dairy cattle.


2021 ◽  
Vol 22 (5) ◽  
pp. 2578
Author(s):  
Trim Lajqi ◽  
Christian Marx ◽  
Hannes Hudalla ◽  
Fabienne Haas ◽  
Silke Große ◽  
...  

Microglia, the innate immune cells of the CNS, exhibit long-term response changes indicative of innate immune memory (IIM). Our previous studies revealed IIM patterns of microglia with opposing immune phenotypes: trained immunity after a low dose and immune tolerance after a high dose challenge with pathogen-associated molecular patterns (PAMP). Compelling evidence shows that innate immune cells adopt features of IIM via immunometabolic control. However, immunometabolic reprogramming involved in the regulation of IIM in microglia has not been fully addressed. Here, we evaluated the impact of dose-dependent microglial priming with ultra-low (ULP, 1 fg/mL) and high (HP, 100 ng/mL) lipopolysaccharide (LPS) doses on immunometabolic rewiring. Furthermore, we addressed the role of PI3Kγ on immunometabolic control using naïve primary microglia derived from newborn wild-type mice, PI3Kγ-deficient mice and mice carrying a targeted mutation causing loss of lipid kinase activity. We found that ULP-induced IIM triggered an enhancement of oxygen consumption and ATP production. In contrast, HP was followed by suppressed oxygen consumption and glycolytic activity indicative of immune tolerance. PI3Kγ inhibited glycolysis due to modulation of cAMP-dependent pathways. However, no impact of specific PI3Kγ signaling on immunometabolic rewiring due to dose-dependent LPS priming was detected. In conclusion, immunometabolic reprogramming of microglia is involved in IIM in a dose-dependent manner via the glycolytic pathway, oxygen consumption and ATP production: ULP (ultra-low-dose priming) increases it, while HP reduces it.


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