Genetic interaction between the tissues of carnation petals as periclinal chimeras

1974 ◽  
Vol 14 (2) ◽  
pp. 109-116 ◽  
Author(s):  
Pierre Pereau-Leroy
2020 ◽  
Vol 9 (3) ◽  
pp. 177-191
Author(s):  
Sridharan Priya ◽  
Radha K. Manavalan

Background: The diseases in the heart and blood vessels such as heart attack, Coronary Artery Disease, Myocardial Infarction (MI), High Blood Pressure, and Obesity, are generally referred to as Cardiovascular Diseases (CVD). The risk factors of CVD include gender, age, cholesterol/ LDL, family history, hypertension, smoking, and genetic and environmental factors. Genome- Wide Association Studies (GWAS) focus on identifying the genetic interactions and genetic architectures of CVD. Objective: Genetic interactions or Epistasis infer the interactions between two or more genes where one gene masks the traits of another gene and increases the susceptibility of CVD. To identify the Epistasis relationship through biological or laboratory methods needs an enormous workforce and more cost. Hence, this paper presents the review of various statistical and Machine learning approaches so far proposed to detect genetic interaction effects for the identification of various Cardiovascular diseases such as Coronary Artery Disease (CAD), MI, Hypertension, HDL and Lipid phenotypes data, and Body Mass Index dataset. Conclusion: This study reveals that various computational models identified the candidate genes such as AGT, PAI-1, ACE, PTPN22, MTHR, FAM107B, ZNF107, PON1, PON2, GTF2E1, ADGRB3, and FTO, which play a major role in genetic interactions for the causes of CVDs. The benefits, limitations, and issues of the various computational techniques for the evolution of epistasis responsible for cardiovascular diseases are exhibited.


1996 ◽  
Vol 157 (4) ◽  
pp. 398-405 ◽  
Author(s):  
Edward J. Klekowski, ◽  
Robin Lowenfeld ◽  
Elizabeth H. Klekowski

2021 ◽  
Vol 1 (2) ◽  
pp. 225-238
Author(s):  
Mohsen Hooshyar ◽  
Daniel Burnside ◽  
Maryam Hajikarimlou ◽  
Katayoun Omidi ◽  
Alexander Jesso ◽  
...  

DNA double-strand breaks (DSBs) are the most deleterious form of DNA damage and are repaired through non-homologous end-joining (NHEJ) or homologous recombination (HR). Repair initiation, regulation and communication with signaling pathways require several histone-modifying and chromatin-remodeling complexes. In budding yeast, this involves three primary complexes: INO80-C, which is primarily associated with HR, SWR1-C, which promotes NHEJ, and RSC-C, which is involved in both pathways as well as the general DNA damage response. Here we identify ARP6 as a factor involved in DSB repair through an RSC-C-related pathway. The loss of ARP6 significantly reduces the NHEJ repair efficiency of linearized plasmids with cohesive ends, impairs the repair of chromosomal breaks, and sensitizes cells to DNA-damaging agents. Genetic interaction analysis indicates that ARP6, MRE11 and RSC-C function within the same pathway, and the overexpression of ARP6 rescues rsc2∆ and mre11∆ sensitivity to DNA-damaging agents. Double mutants of ARP6, and members of the INO80 and SWR1 complexes, cause a significant reduction in repair efficiency, suggesting that ARP6 functions independently of SWR1-C and INO80-C. These findings support a novel role for ARP6 in DSB repair that is independent of the SWR1 chromatin remodeling complex, through an apparent RSC-C and MRE11-associated DNA repair pathway.


Sign in / Sign up

Export Citation Format

Share Document