Salinity tolerance mechanisms and their breeding implications

Abstract Background The era of first green revolution brought about by the application of chemical fertilizers surely led to the explosion of food grains, but left behind the notable problem of salinity. Continuous application of these fertilizers coupled with fertilizer-responsive crops make the country self-reliant, but continuous deposition of these led to altered the water potential and thus negatively affecting the proper plant functioning from germination to seed setting. Main body Increased concentration of anion and cations and their accumulation and distribution cause cellular toxicity and ionic imbalance. Plants respond to salinity stress by any one of two mechanisms, viz., escape or tolerate, by either limiting their entry via root system or controlling their distribution and storage. However, the understanding of tolerance mechanism at the physiological, biochemical, and molecular levels will provide an insight for the identification of related genes and their introgression to make the crop more resilient against salinity stress. Short conclusion Novel emerging approaches of plant breeding and biotechnologies such as genome-wide association studies, mutational breeding, marker-assisted breeding, double haploid production, hyperspectral imaging, and CRISPR/Cas serve as engineering tools for dissecting the in-depth physiological mechanisms. These techniques have well-established implications to understand plants’ adaptions to develop more tolerant varieties and lower the energy expenditure in response to stress and, constitutively fulfill the void that would have led to growth resistance and yield penalty.

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A review on association and correlation of genetic variants with eating disorders and obesity

Future Journal of Pharmaceutical Sciences ◽

10.1186/s43094-021-00250-2 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Sayed Koushik Ahamed ◽

Md Abdul Barek ◽

Uthpall Kumar Roy ◽

Md Kouser ◽

Md Sharif Reza ◽

...

Keyword(s):

Eating Disorders ◽

Eating Disorder ◽

Association Studies ◽

Main Body ◽

Genome Wide Association Studies ◽

Addictive Behaviors ◽

Future Directions ◽

Mortality And Morbidity ◽

Genome Wide ◽

Significant Mortality

Abstract Background Now, eating disorders and obesity and their correlations are danger signal in worldwide which is caused by multifactor and associated with significant mortality and morbidity. Main body Every aspect of a patient’s life is influenced by eating disorders and obesity and their correlations. Due to frequent seeing of obese patients, eating disorders have been included in the review as they can sometimes be associated with obesity. However, it should be noted that most patients having eating disorder are at risk to be obese or overweight. This research explores the risk factors for the two disorders, as well as the assessment of medical complications and treatment recommendations for the disorders. In these two disorders, there is also a correlation. The essential consideration is that eating disorders are impulse-control disorders which are similar to addictive behaviors in some aspects. So it is a crying need to treat a patient with obesity and eating disorders simultaneously to ensure success. Genome-wide association studies (GWASs) have increased our knowledge of the pathophysiology of eating disorders (EDs) and obesity and their correlation. Conclusion This review enlightens on the summary of eating disorder, obesity, genotypic traits, molecular relations, interaction, correlation, and effect of eating disorder and obesity which outline potential future directions and clinical implications for patients with EDs and obesity.

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Association of genetic variants with prostate cancer in Africa: a concise review

Egyptian Journal of Medical Human Genetics ◽

10.1186/s43042-021-00157-w ◽

2021 ◽

Vol 22 (1) ◽

Author(s):

Emmanuel Acheampong ◽

Evans Asamoah Adu ◽

Christian Obirikorang ◽

George Amoah ◽

Osei Owusu Afriyie ◽

...

Keyword(s):

Prostate Cancer ◽

Genetic Variants ◽

Association Studies ◽

African Ancestry ◽

Candidate Gene Approach ◽

Main Body ◽

Genome Wide Association Studies ◽

Genetic Associations ◽

Genetic Studies ◽

Genome Wide

Abstract Background Prostate cancer (PCa) has one of the highest heritability of all major cancers, where the genetic contribution has been documented, and knowledge about the molecular genetics of the disease is increasing. However, the extent and aspects to which genetic variants explain PCa heritability in Africa are limited. Main body In this review, we summarize studies that highlight how identified genetic variants explain differences in PCa incidence and presentation across ethnic groups. We also present the knowledge gaps in PCa genetics in Africa and why Africa represents an untapped potential ground for genetic studies on PCa. A significant number of genome-wide association studies, linkage, and fine-mapping analyses have been conducted globally, and that explains 30–33% of PCa heritability. The African ancestry has a significant mention in PCa incidence and presentation. To date, the candidate gene approach has replicated 23 polymorphisms including dinucleotide and trinucleotide repeats in 16 genes. CYP17-rs743572, CYP3A4-rs2740574, CYP3A5-rs776746, CYP3A43-rs501275, and haplotype blocks, containing these variants, are significantly associated with PCa among some population groups but not others. With the few existing studies, the extent of genetic diversity in Africa suggests that genetic associations of PCa to African ancestry go beyond nucleotide sequence polymorphisms, to a level of environmental adaptation, which may interpret genetic risk profiles. Also, the shreds of evidence suggest that evolutionary history contributes to the high rates of PCa relative to African ancestry, and genetic associations do not always replicate across populations. Conclusion The genetic architecture of PCa in Africa provides important contributions to the global understanding of PCa specifically the African-ancestry hypothesis. There is a need for more prostate cancer consortiums to justify the heritable certainties of PCa among Africans, and emphasis should be placed on the genetic epidemiological model of PCa in Africa.

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G6PC2 Modulates Fasting Blood Glucose In Male Mice in Response to Stress

Endocrinology ◽

10.1210/en.2016-1245 ◽

2016 ◽

Vol 157 (8) ◽

pp. 3002-3008 ◽

Cited By ~ 7

Author(s):

Kayla A. Boortz ◽

Kristen E. Syring ◽

Chunhua Dai ◽

Lynley D. Pound ◽

James K. Oeser ◽

...

Keyword(s):

Association Studies ◽

Fasting Blood Glucose ◽

Genome Wide Association ◽

Genome Wide Association Studies ◽

Nucleotide Polymorphisms ◽

Single Nucleotide ◽

Genome Wide ◽

Response To Stress ◽

Fasting Plasma Insulin ◽

The Difference

The glucose-6-phosphatase catalytic 2 (G6PC2) gene is expressed specifically in pancreatic islet beta cells. Genome-wide association studies have shown that single nucleotide polymorphisms in the G6PC2 gene are associated with variations in fasting blood glucose (FBG) but not fasting plasma insulin. Molecular analyses examining the functional effects of these single nucleotide polymorphisms demonstrate that elevated G6PC2 expression is associated with elevated FBG. Studies in mice complement these genome-wide association data and show that deletion of the G6pc2 gene lowers FBG without affecting fasting plasma insulin. This suggests that, together with glucokinase, G6PC2 forms a substrate cycle that determines the glucose sensitivity of insulin secretion. Because genome-wide association studies and mouse studies demonstrate that elevated G6PC2 expression raises FBG and because chronically elevated FBG is detrimental to human health, increasing the risk of type 2 diabetes, it is unclear why G6PC2 evolved. We show here that the synthetic glucocorticoid dexamethasone strongly induces human G6PC2 promoter activity and endogenous G6PC2 expression in isolated human islets. Acute treatment with dexamethasone selectively induces endogenous G6pc2 expression in 129SvEv but not C57BL/6J mouse pancreas and isolated islets. The difference is due to a single nucleotide polymorphism in the C57BL/6J G6pc2 promoter that abolishes glucocorticoid receptor binding. In 6-hour fasted, nonstressed 129SvEv mice, deletion of G6pc2 lowers FBG. In response to the stress of repeated physical restraint, which is associated with elevated plasma glucocorticoid levels, G6pc2 gene expression is induced and the difference in FBG between wild-type and knockout mice is enhanced. These data suggest that G6PC2 may have evolved to modulate FBG in response to stress.

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