Background
Early embryonic mortality is one of the major intriguing factors of reproductive failure that causes considerable challenge to the mammalian cell biologists. Heat stress is the major ...factor responsible for reduced fertility in farm animals. The present study aimed to investigate the influence of heat stress on prostaglandin production and the expression of key genes, including
COX-2
,
PGES
,
PGFS
,
ITGAV
and
LGALS15
, in buffalo endometrial epithelial cells.
Methods and results
Buffalo genitalia containing ovaries with corpus luteum (CL) were collected immediately post-slaughter. The stages of the estrous cycle were determined based on macroscopic observations of the ovaries. Uterine lumens of the mid-luteal phase (days 6–10 of the estrous cycle) were washed and treated with trypsin to isolate epithelial cells, which were then cultured at control temperature (38.5 °C for 24 h) or exposed to elevated temperatures 38.5 °C for 6 h, 40.5 °C for 18 h; Heat Stressed (HS). The supernatant and endometrial epithelial cells were collected at various time points (0, 3, 6, 12, and 24 h) from both the control and treatment groups. Although heat stress (40.5 °C) significantly (
P
< 0.05) increased
COX-2
,
PGES
, and
PGFS
transcripts in epithelial cells but it did not affect the in vitro production of PGF
2α
and PGE
2
. The expression of
ITGAV
and
LGALS15
mRNAs in endometrial epithelial cells remained unaltered under elevated temperature conditions.
Conclusion
It can be concluded that elevated temperature did not directly modulate prostaglandin production but, it promoted the expression of
COX-2
,
PGES
and
PGFS
mRNA in buffalo endometrial epithelial cells.
Abnormal activation of insulin-like growth factor (IGF)-Akt signaling is implicated in the development of various diseases, including heart failure. However, the molecular mechanisms that regulate ...activation of this signaling pathway are not completely understood. Here we show that sirtuin 6 (SIRT6), a nuclear histone deacetylase, functions at the level of chromatin to directly attenuate IGF-Akt signaling. SIRT6-deficient mice developed cardiac hypertrophy and heart failure, whereas SIRT6 transgenic mice were protected from hypertrophic stimuli, indicating that SIRT6 acts as a negative regulator of cardiac hypertrophy. SIRT6-deficient mouse hearts showed hyperactivation of IGF signaling-related genes and their downstream targets. Mechanistically, SIRT6 binds to and suppresses the promoter of IGF signaling-related genes by interacting with c-Jun and deacetylating histone 3 at Lys9 (H3K9). We also found reduced SIRT6 expression in human failing hearts. These findings disclose a new link between SIRT6 and IGF-Akt signaling and implicate SIRT6 in the development of cardiac hypertrophy and failure.
The progress of leaf rust research in wheat Prasad, Pramod; Savadi, Siddanna; Bhardwaj, S.C. ...
Fungal biology,
June 2020, 2020-Jun, 2020-06-00, 20200601, Letnik:
124, Številka:
6
Journal Article
Recenzirano
Leaf rust (also called brown rust) in wheat, caused by fungal pathogen Puccinia triticina Erikss. (Pt) is one of the major constraints in wheat production worldwide. Pt is widespread with diverse ...population structure and undergoes rapid evolution to produce new virulent races against resistant cultivars that are regularly developed to provide resistance against the prevailing races of the pathogen. Occasionally, the disease may also take the shape of an epidemic in some wheat-growing areas causing major economic losses. In the recent past, substantial progress has been made in characterizing the sources of leaf rust resistance including non-host resistance (NHR). Progress has also been made in elucidating the population biology of Pt and the mechanisms of wheat-Pt interaction. So far, ∼80 leaf rust resistance genes (Lr genes) have been identified and characterized; some of them have also been used for the development of resistant wheat cultivars. It has also been shown that a gene-for-gene relationship exists between individual wheat Lr genes and the corresponding Pt Avr genes so that no Lr gene can provide resistance unless the prevailing race of the pathogen carries the corresponding Avr gene. Several Lr genes have also been cloned and their products characterized, although no Avr gene corresponding a specific Lr gene has so far been identified. However, several candidate effectors for Pt have been identified and functionally characterized using genome-wide analyses, transcriptomics, RNA sequencing, bimolecular fluorescence complementation (BiFC), virus-induced gene silencing (VIGS), transient expression and other approaches. This review summarizes available information on different aspects of the pathogen Pt, genetics/genomics of leaf rust resistance in wheat including cloning and characterization of Lr genes and epigenetic regulation of disease resistance.
•Wheat leaf rust (WLR) is one of the major constraints to wheat production.•∼80 Lr genes have been identified and used in breeding.•Molecular basis of wheat-Pt interaction has been discovered in several cases.•Nature of Lr genes & their interaction with effectors are being interpreted.•The review discusses QTLs, Pt biology, genomics, effectoromics, epigenetics.
Honokiol (HKL) is a natural biphenolic compound derived from the bark of magnolia trees with anti-inflammatory, anti-oxidative, anti-tumour and neuroprotective properties. Here we show that HKL ...blocks agonist-induced and pressure overload-mediated, cardiac hypertrophic responses, and ameliorates pre-existing cardiac hypertrophy, in mice. Our data suggest that the anti-hypertrophic effects of HKL depend on activation of the deacetylase Sirt3. We demonstrate that HKL is present in mitochondria, enhances Sirt3 expression nearly twofold and suggest that HKL may bind to Sirt3 to further increase its activity. Increased Sirt3 activity is associated with reduced acetylation of mitochondrial Sirt3 substrates, MnSOD and oligomycin-sensitivity conferring protein (OSCP). HKL-treatment increases mitochondrial rate of oxygen consumption and reduces ROS synthesis in wild type, but not in Sirt3-KO cells. Moreover, HKL-treatment blocks cardiac fibroblast proliferation and differentiation to myofibroblasts in a Sirt3-dependent manner. These results suggest that HKL is a pharmacological activator of Sirt3 capable of blocking, and even reversing, the cardiac hypertrophic response.
Wheat production and productivity in the past witnessed a remarkable growth. However, this growth rate could not be sustained during the last decade, causing concern among world wheat community. ...Marker-assisted selection (MAS), which is being practiced for improvement of a variety of traits in wheat around the world, may at least partly help in providing the desired solution. Marker-trait associations are now known for a number of simple, but difficult-to-score traits, so that MAS has been found useful for improvement of several of these important economic traits. Breeding strategies including marker-assisted backcrossing, forward breeding, MAS involving doubled haploid technology and F₂ enrichment have been successfully utilized for this purpose. However, for improvement of complex polygenic traits, newer technologies based on high throughput genotyping associated with new marker systems (e.g., DArT and SNP), and new selection strategies such as AB-QTL, mapping-as-you-go, marker-assisted recurrent selection and genome-wide selection will have to be tried in future. The progress made in all these aspects of marker-assisted wheat breeding, and the limitations and future prospects of this emerging technology have been reviewed in this article.
Continuous generation of plastic waste has prompted substantial research efforts in its utilization as a feedstock for energy generation. Pyrolysis has emerged as one of the best waste management ...technique for energy extraction from the plastic waste. The objective of this work is to investigate the effect of operating temperature on the liquid product yields in the pyrolysis process by non-isothermal heating. Non-catalytic thermal pyrolysis of waste polyethylene (PE) high density polyethylene (HDPE), waste polypropene (PP), waste polystyrene (PS), waste polyethylene terephthalate (PET) and mixed plastic waste (MPW) was carried out in a non-sweeping atmosphere in a semi-batch reactor at four different temperatures 450, 500, 550, and 600 °C. The minimum degradation temperature of the mixed and individual plastics was obtained using a thermogravimetric apparatus (TGA) at a heating rate of 20 °C/min. The TGA results show that all plastics degrade in a single step and the degradation temperatures of PS > PET > PP > HDPE, while mixed plastic degradation indicates two distinct degradation steps. Further, a waste polymer shows a lower degradation temperature than the virgin polymer. The degradation of HDPE is found to produce the maximum oil yield with minimum solid residue. The degradation of PET results in the highest amount of solid and benzoic acid as crystals and gas with no oil. Degradation of mixed plastic causes oil yield in the intermediate range of pyrolysis of individual plastic wastes. Overall, 500 °C is observed to be an optimum temperature for the recovery of low-density pyrolytic oil with the highest liquid yield. The degradation of PE and PP is found to be caused by random chain scission followed by inter and intramolecular hydrogen transfer. The degradation of PS occurs by side elimination or end chain scission followed by β-scission mechanism. The degradation of mix plastics results from random chain scission followed by β-scission mechanism. The effect of temperature on oil and gas recovery as well as recovery time was also assessed.
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•Effect of temperature on bulk pyrolysis of plastic wastes.•Impact of recycling on thermal degradation of waste plastics.•Comparative analysis of thermal degradation of waste and virgin plastics.•Time and temperature based evolution profile of pyrolytic products.•Elaborated discussion on degradation mechanism of different waste plastics.
The present study assessed the effects of supplementation of different antioxidants on oocyte maturation, embryo production, reactive oxygen species (ROS) production and expression of key ...developmental genes. In this study, using ovine as an animal model, we tested the hypothesis that antioxidant supplementation enhanced the developmental competence of oocytes. Ovine oocytes aspirated from local abattoir-derived ovaries were subjected to IVM with different concentrations of antioxidants (Melatonin, Ascorbic acid (Vit C), alpha-tocopherol (Vit E), Sodium selenite (SS). Oocytes matured without any antioxidant supplementation were used as controls. The oocytes were assessed for maturation rates and ROS levels. Further, embryo production rates in terms of cleavage, blastocysts and total cell numbers were evaluated after performing in vitro fertilization. Real-Time PCR analysis was used to evaluate the expression of stress related gene (SOD-1), growth related (GDF-9, BMP-15), and apoptosis-related genes (BCL-2 and BAX). We observed that maturation rates were significantly higher in alpha-tocopherol (100 μM; 92.4%) groups followed by melatonin (30 μM; 89.1%) group. However, blastocyst rates in ascorbic acid (100 μM; 19.5%), melatonin (30 μM; 18.4%), alpha-tocopherol (100 μM; 18.2%), and sodium selenite (20 μM; 16.9%) groups were significantly higher (P 0.05) than that observed in the control groups. Total cell numbers in blastocysts in the melatonin, ascorbic acid and alpha-tocopherol groups were significantly higher than those observed in sodium selenite and control groups. ROS production was reduced in groups treated with melatonin (30 μM), vitamin C (100 μM), sodium selenite (20 μM) and α-tocopherol (200 μM) compared with that observed in the control group. Supplementation of antioxidants caused the alterations in mRNA expression of growth, stress, and apoptosis related gene expression in matured oocytes. The results recommend that antioxidants alpha-tocopherol (200 μM), sodium selenite (40 μM), melatonin (30 μM) and ascorbic acid (100 μM) during IVM reduced the oxidative stress by decreasing ROS levels in oocytes, thus improving embryo quantity and quality.
•Supplementation of different antioxidants on oocyte development and expression of key developmental genes were studied.•Total cell numbers in blastocysts in the melatonin, ascorbic acid and alpha-tocopherol treated groups were significantly higher than those observed in sodium selenite treated and control groups.•Antioxidants viz. alpha-tocopherol (200 μM), sodium selenite (40 μM), melatonin (30 μM) and ascorbic acid (100 μM) during IVM improved thr embryo quantity and quality.
DNA polymerase theta (Pol θ)-mediated end joining (TMEJ) has been implicated in the repair of chromosome breaks, but its cellular mechanism and role relative to canonical repair pathways are poorly ...understood. We show that it accounts for most repairs associated with microhomologies and is made efficient by coupling a microhomology search to removal of non-homologous tails and microhomology-primed synthesis across broken ends. In contrast to non-homologous end joining (NHEJ), TMEJ efficiently repairs end structures expected after aborted homology-directed repair (5′ to 3′ resected ends) or replication fork collapse. It typically does not compete with canonical repair pathways but, in NHEJ-deficient cells, is engaged more frequently and protects against translocation. Cell viability is also severely impaired upon combined deficiency in Pol θ and a factor that antagonizes end resection (Ku or 53BP1). TMEJ thus helps to sustain cell viability and genome stability by rescuing chromosome break repair when resection is misregulated or NHEJ is compromised.
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•Pol θ directs end joining by coupling a microhomology search to synthesis across ends•Pol θ-mediated end joining is critical when either canonical repair pathway fails•Pol θ is also essential when cells aberrantly regulate resection of chromosome breaks•Pol θ-dependent repair can both suppress and promote genome instability
Wyatt et al. show that Polymerase θ accounts for most microhomology-dependent chromosome break repair and outline a mechanism that makes this pathway efficient and flexible. They define biologically relevant substrates, determine that it is essential in cells that inappropriately regulate resection, and show that it can both positively and negatively affect genome stability.
Abstract Myosin is a molecular motor, which interacts with actin to convert the energy from ATP hydrolysis into mechanical work. In cardiac myocytes, two myosin isoforms are expressed and their ...relative distribution changes in different developmental and pathophysiologic conditions of the heart. It has been realized for a long time that a shift in myosin isoforms plays a major role in regulating myocardial contractile activity. With the recent evidence implicating that alteration in myosin isoform ratio may be eventually beneficial for the treatment of a stressed heart, a new interest has developed to find out ways of controlling the myosin isoform shift. This article reviews the published data describing the role of myosin isoforms in the heart and highlighting the importance of various factors shown to influence myosin isofrom shift during physiology and disease states of the heart.
DNA polymerase theta mediates an end joining pathway (TMEJ) that repairs chromosome breaks. It requires resection of broken ends to generate long, 3′ single-stranded DNA tails, annealing of ...complementary sequence segments (microhomologies) in these tails, followed by microhomology-primed synthesis sufficient to resolve broken ends. The means by which microhomologies are identified is thus a critical step in this pathway, but is not understood. Here we show microhomologies are identified by a scanning mechanism initiated from the 3′ terminus and favoring bidirectional progression into flanking DNA, typically to a maximum of 15 nucleotides into each flank. Polymerase theta is frequently insufficiently processive to complete repair of breaks in microhomology-poor, AT-rich regions. Aborted synthesis leads to one or more additional rounds of microhomology search, annealing, and synthesis; this promotes complete repair in part because earlier rounds of synthesis generate microhomologies de novo that are sufficiently long that synthesis is more processive. Aborted rounds of synthesis are evident in characteristic genomic scars as insertions of 3 to 30 bp of sequence that is identical to flanking DNA (“templated” insertions). Templated insertions are present at higher levels in breast cancer genomes from patients with germline BRCA1/2 mutations, consistent with an addiction to TMEJ in these cancers. Our work thus describes the mechanism for microhomology identification and shows how it both mitigates limitations implicit in the microhomology requirement and generates distinctive genomic scars associated with pathogenic genome instability.
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