Analysis of relationship between key genes and astaxanthin biosynthesis in Phaffia rhodozyma by transcript level and gene knock-out

2019 ◽  
Author(s):  
Zhipeng Li ◽  
Lina Chen ◽  
Tianli Li ◽  
Xiping Du ◽  
Ning He ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Transcript Level ◽  
Phaffia Rhodozyma ◽  
Knock Out ◽  
Astaxanthin Production ◽  
Key Genes ◽  
Different Strains ◽  
The Relationship ◽  
Rate Limiting ◽  
Exact Relationship

Abstract Background Phaffia rhodozyma is a potential industrial source for production of natural astaxanthin. The synthetic mechanism of astaxanthin in P. rhodozyma is complex and unclear that blocked its development. Results In this study, eight genes related to dicyclic and monocyclic pathway in three different strains of P. rhodozyma were analyzed, and the relationship between the expression and astaxanthin biosynthesis was explored. Among these genes, crtYB (R=0.75, P<0.05) and asy genes (R=0.74, P<0.05) showed the most closely correlation with astaxanthin biosynthesis. In order to further study exact relationship, crtYB and asy genes were knocked out by homologous recombination. After crtYB knock-out, astaxanthin was decreased to be under detected line. It suggested crtYB played a role in dicyclic and monocyclic pathway. Meanwhile, the asy gene was in dicyclic pathway of astaxanthin biosynthesis, and its knock-out would promote the astaxanthin biosynthesis in monocyclic pathway, resulting in a 25.04% increase in astaxanthin production. Conclusion The possible rate-limiting enzymes were asy gene and crtYB illustrated by analysis of regression. Knock-out of asy and crtYB gene was great helpful to understand the synthetic pathway of astaxanthin, and significant to the industrial application of producing astaxanthin.

The role of key genes in astaxanthin biosynthesis in Phaffia rhodozyma by transcript level and gene knockout

2021 ◽  
Author(s):  
Zhipeng Li ◽  
Lina Chen ◽  
Haoyi Yang ◽  
Tianli Li ◽  
Xiping Du ◽  
...  
Keyword(s):  
Gene Knockout ◽  
Transcript Level ◽  
Phaffia Rhodozyma ◽  
Key Genes

scholarly journals The search for homology does not limit the rate of extrachromosomal homologous recombination in mammalian cells.

Genetics ◽  
1994 ◽  
Vol 136 (2) ◽  
pp. 597-605
Author(s):  
A S Waldman
Keyword(s):  
Homologous Recombination ◽  
Dna Sequences ◽  
Mammalian Cells ◽  
Insertion Mutant ◽  
Insertion Mutation ◽  
Homologous Pairing ◽  
Rate Limiting Step ◽  
Limiting Step ◽  
Homology Searching ◽  
Rate Limiting

Abstract Mouse LTK- cells were transfected with a pair of defective Herpes simplex virus thymidine kinase (tk) genes. One tk gene had an 8-bp insertion mutation while the second gene had a 100-bp inversion. Extrachromosomal homologous recombination leading to the reconstruction of a functional tk gene was monitored by selecting for tk positive cells using medium supplemented with hypoxanthine/aminopterin/thymidine. To assess whether the search for homology may be a rate-limiting step of recombination, we asked whether the presence of an excess number of copies of a tk gene possessing both the insertion and inversion mutations could inhibit recombination between the singly mutated tk genes. Effective competitive inhibition would require that homology searching (homologous pairing) occur rapidly and efficiently. We cotransfected plasmid constructs containing the singly mutated genes in the presence or absence of competitor sequences in various combinations of linear or circular forms. We observed effective inhibition by the competitor DNA in six of the seven combinations studied. A lack of inhibition was observed only when the insertion mutant gene was cleaved within the insertion mutation and cotransfected with the two other molecules in circular form. Additional experiments suggested that homologous interactions between two DNA sequences may compete in trans with recombination between two other sequences. We conclude that homology searching is not a rate-limiting step of extrachromosomal recombination in mammalian cells. Additionally, we speculate that a limiting factor is involved in a recombination step following homologous pairing and has a high affinity for DNA termini.

scholarly journals Cortical RORβ is required for layer 4 transcriptional identity and barrel integrity

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Erin A Clark ◽  
Michael Rutlin ◽  
Lucia Capano ◽  
Samuel Aviles ◽  
Jordan R Saadon ◽  
...  
Keyword(s):  
Binding Sites ◽  
Binding Capacity ◽  
Chromatin Accessibility ◽  
Excitatory Input ◽  
Orphan Receptor ◽  
Knock Out ◽  
Putative Target ◽  
Layer 4 ◽  
The Relationship ◽  
Receptor Beta

Retinoic acid-related orphan receptor beta (RORβ) is a transcription factor (TF) and marker of layer 4 (L4) neurons, which are distinctive both in transcriptional identity and the ability to form aggregates such as barrels in rodent somatosensory cortex. However, the relationship between transcriptional identity and L4 cytoarchitecture is largely unknown. We find RORβ is required in the cortex for L4 aggregation into barrels and thalamocortical afferent (TCA) segregation. Interestingly, barrel organization also degrades with age in wildtype mice. Loss of RORβ delays excitatory input and disrupts gene expression and chromatin accessibility, with down-regulation of L4 and up-regulation of L5 genes, suggesting a disruption in cellular specification. Expression and binding site accessibility change for many other TFs, including closure of neurodevelopmental TF binding sites and increased expression and binding capacity of activity-regulated TFs. Lastly, a putative target of RORβ, Thsd7a, is down-regulated without RORβ, and Thsd7a knock-out alone disrupts TCA organization in adult barrels.

Carbon dioxide excretion in fishes

1986 ◽  
Vol 64 (3) ◽  
pp. 565-572 ◽  
Author(s):  
S. F. Perry
Keyword(s):  
Carbon Dioxide ◽  
Minor Amount ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Convective Processes ◽  
Adrenergic Control ◽  
And Control ◽  
The Relationship ◽  
Rate Limiting ◽  
Subsequent Diffusion

The pattern and control of carbon dioxide excretion in fish is reviewed with particular emphasis on the site(s) of bicarbonate dehydration, the involvement of diffusive and convective processes, and the relationship with ionic and acid–base regulation. The principal route for carbon dioxide excretion in fish involves the catalysed dehydration of plasma bicarbonate within erythrocytes to form physically dissolved CO2 and the subsequent diffusion of physically dissolved CO2 across the gill epithelium. It is likely that bicarbonate entry into the erythrocyte in exchange for intracellular chloride, rather than branchial CO2 diffusion or blood/water convection, is the rate-limiting process in carbon dioxide excretion, although a change in any one of these factors will affect overall CO2 elimination. Additionally, a relatively minor amount of CO2 is hydrated within gill epithelial cells to form H+ and HCO3− ions that are exchanged for Cl− ions and Na+ ions, respectively. Evidence is presented indicating that branchial and erythrocytic HCO3−/Cl− exchanges are under adrenergic control and that modulations of these processes by elevated levels of circulating catecholamines may be important in regulating acid–base disturbances.

Genomic DNA methylation analysis revealed that BLNK is a key potential gene in the regulation of autophagy-related thyroid cancer progression

Genome ◽  
2021 ◽  
Author(s):  
Shengchi Zhang ◽  
Yongzhe Zheng ◽  
Guimin Zhang ◽  
Peng Lin ◽  
Wei Wang
Keyword(s):  
Dna Methylation ◽  
Thyroid Cancer ◽  
Cancer Progression ◽  
Protein Interactions ◽  
Methylation Status ◽  
Expression Change ◽  
Prognostic Analysis ◽  
Key Genes ◽  
New Perspective ◽  
The Relationship

The purpose of this study was to explore the relationship between autophagy and DNA methylation, and to identify key genes for autophagy-regulated thyroid cancer progression. We divided patients with thyroid cancer into high-autophagy score (AS) group and low-AS group based on their AS values. The results found that AS was associated with the distant metastasis of thyroid cancer, and adversely affected prognosis. Then, we screened 359 differently expressed genes (DEGs) with DNA methylation status consistent with gene expression change. Functional classification analysis demonstrated that the 359 DEGs consistent with DNA methylation status were significantly involved in adhesion, migration and differentiation of immune cells. To further screen the key genes in the autophagy-related thyroid cancer progression, we constructed a protein-protein interactions (PPI) network and performed prognostic analysis. B cell linker (BLNK) was identified as the key potential gene affecting autophagy-related thyroid cancer progression. Finally, we verified that BLNK promoted the proliferation of thyroid cancer cells, and BLNK expression was regulated by DNA methylation. Our research provides a new perspective for exploring the relationship between autophagy and DNA methylation during the progression of thyroid cancer, and provides a new target for the treatment of metastatic thyroid cancer.

scholarly journals Heme Oxygenases: Cellular Multifunctional and Protective Molecules against UV-Induced Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
ShiDa Chen ◽  
XiaoYu Wang ◽  
Muhammad Farrukh Nisar ◽  
Mao Lin ◽  
Julia Li Zhong
Keyword(s):  
Disease Progression ◽  
Heme Oxygenase ◽  
Skin Diseases ◽  
Functional Differentiation ◽  
Heme Oxygenase 1 ◽  
Signal Molecule ◽  
Splice Isoform ◽  
The Relationship ◽  
Rate Limiting

Ultraviolet (UV) irradiation can be considered as a double-edged sword: not only is it a crucial environmental factor that can cause skin-related disorders but it can also be used for phototherapy of skin diseases. Inducible heme oxygenase-1 (HO-1) in response to a variety of stimuli, including UV exposure, is vital to maintain cell homeostasis. Heme oxygenase-2 (HO-2), another member of the heme oxygenase family, is constitutively expressed. In this review, we discuss how heme oxygenase (HO), a vital rate-limiting enzyme, participates in heme catabolism and cytoprotection. Phylogenetic analysis showed that there may exist a functional differentiation between HO-1 and HO-2 during evolution. Furthermore, depending on functions in immunomodulation and antioxidation, HO-1 participates in disease progression, especially in pathogenesis of skin diseases, such as vitiligo and psoriasis. To further investigate the particular role of HO-1 in diseases, we summarized the profile of the HO enzyme system and its related signaling pathways, such as Nrf2 and endoplasmic reticulum crucial signaling, both known to regulate HO-1 expression. Furthermore, we report on a C-terminal truncation of HO-1, which is generally considered as a signal molecule. Also, a newly identified alternative splice isoform of HO-1 not only provides us a novel perspective on comprehensive HO-1 alternative splicing but also offers us a basis to clarify the relationship between HO-1 transcripts and oxidative diseases. To conclude, the HO system is not only involved in heme catabolism but also involved in biological processes related to the pathogenesis of certain diseases, even though the mechanism of disease progression still remains sketchy. Further understanding the role of the HO system and its relationship to UV is helpful for revealing the HO-related signaling networks and the pathogenesis of many diseases.

scholarly journals The Saccharomyces cerevisiae Rad6 Postreplication Repair and Siz1/Srs2 Homologous Recombination-Inhibiting Pathways Process DNA Damage That Arises in asf1 Mutants

2009 ◽  
Vol 29 (19) ◽  
pp. 5226-5237 ◽  
Author(s):  
Ellen S. Kats ◽  
Jorrit M. Enserink ◽  
Sandra Martinez ◽  
Richard D. Kolodner
Keyword(s):  
Homologous Recombination ◽  
Genome Stability ◽  
Chromosomal Rearrangements ◽  
Nuclear Antigen ◽  
Recombination Suppression ◽  
Postreplication Repair ◽  
Gross Chromosomal Rearrangements ◽  
Translesion Bypass ◽  
The Relationship ◽  
Proliferating Cell

ABSTRACT The Asf1 and Rad6 pathways have been implicated in a number of common processes such as suppression of gross chromosomal rearrangements (GCRs), DNA repair, modification of chromatin, and proper checkpoint functions. We examined the relationship between Asf1 and different gene products implicated in postreplication repair (PRR) pathways in the suppression of GCRs, checkpoint function, sensitivity to hydroxyurea (HU) and methyl methanesulfonate (MMS), and ubiquitination of proliferating cell nuclear antigen (PCNA). We found that defects in Rad6 PRR pathway and Siz1/Srs2 homologous recombination suppression (HRS) pathway genes suppressed the increased GCR rates seen in asf1 mutants, which was independent of translesion bypass polymerases but showed an increased dependency on Dun1. Combining an asf1 deletion with different PRR mutations resulted in a synergistic increase in sensitivity to chronic HU and MMS treatment; however, these double mutants were not checkpoint defective, since they were capable of recovering from acute treatment with HU. Interestingly, we found that Asf1 and Rad6 cooperate in ubiquitination of PCNA, indicating that Rad6 and Asf1 function in parallel pathways that ubiquitinate PCNA. Our results show that ASF1 probably contributes to the maintenance of genome stability through multiple mechanisms, some of which involve the PRR and HRS pathways.

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