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  • ISSN: 2334-1823
    Current Issue
    Volume 4, Issue 1
    Review Article
    Raquel Caserta*and Alessandra Alves de Souza
    Since manipulation of DNA sequences was feasible, it has also become feasible to insert such sequences into distinct genomes. The possibility of creating plants with completely new characteristics conferred by one or more genetic sequences is undoubtedly an exciting platform to be explored, and for sure, a point of divergence between to accept or to deny such new variations created. Currently, several products present new traits ranging from insects resistance to vaccine synthesis, and the technique is still a subject of great criticism. Different nomenclatures are adopted for plants that had their genome altered and in this work they will be named genetically modified plants, which encloses plants presenting traits from non-related organisms such as viruses and bacteria, as well as plants belonging to the new concepts of cisgenic and intragenic. These concepts were created due to the possibility of obtaining isolated genes containing their own regulatory elements or genetic combinations between plant regulatory sequences and target genes, allowing the cisgenic technique to be partially considered an improvement on the classical reproduction technique. In this review we will discuss the three generations of GMs developed, as well as the recent questions about the concept of cisgenic and intragenic, and how these new approaches on genome engineered plants can collaborate to overcome public acceptance of an increasing in availability of GM foods for consumers.
    Umesh Gangishetti and William G. Kelly*
    Mounting evidence suggests that environmental exposures in one generation may result in changes in gene expression that are heritable for multiple generations, yet are unaccompanied by genetic mutations. These phenomena are considered to be the result of epigenetic mechanisms, which can establish metastable states of chromatin-based genome architecture that can be passed through the gametes into subsequent generations. Such heritability requires that normally transient epigenetic changes become stabilized in the germline and become part of the information that is passed from one generation to the next. Work in the genetic model organism Caenorhabditis elegans has uncovered a number of mechanisms that influence transgenerational epigenetic inheritance. These include non-coding RNA-based mechanisms that target genomic loci for heritable repression through the recruitment of histone modifiers. Less understood is how heritable gene activation may be established and maintained. In this review we summarize results that indicate that a network of antagonistic chromatin modifying activities may help maintain heritable gene transcription in the germline of C. elegans. Chief among these activities may be RNA Polymerase II, and the histone methyl transferases with which it is associated, which “mark” regions of transcriptional activity in germ cell chromatin. These patterns are then further maintained by transcription-independent mechanisms that are essential for germline function in subsequent generations.
    Esma Sarikaya*
    Turner syndrome (TS), is the most common chromosomal abnormality in females. TS is caused by haploinsufficiency of the short arm of X-chromosome, and is usually diagnosed by karyotyping which is time-consuming, expensive and unfeasible for population screening. Neonatal diagnosis of TS permits detection of associated malformations, appropriate therapy for short stature and puberty, thus improving patient quality of life and minimizing sequels. However fewer than 20% of the cases are diagnosed during the neonatal period. TS is not currently part of newborn screening. A considerable delay in diagnosing girls with TS is obvious. The use of combined molecular-cytogenetic approaches in different tissues of different embryological origins would be of help for thedetection of mosaic TS patients. Simpler, faster and less expensive new methods are needed for population screening programmes.
    Kathirvel Renugadevi, Asim Kumar Sil, Perumalsamy Vijayalakshmi, and PeriasamySundaresan1*
    Albinism is one of the major metabolic disorders due to tyrosinase deficiency in the body, thus leads to defect in the production of melanin biosynthesis and leads to lack of pigmentation in ocular & cutaneous region is called as oculo cutaneous albinism and lack of melanin in ocular region alone is known as ocular albinism. In this genetic study, performed the candidate gene analysis for TYR, P, MC1R, TYRP1, MATP1 and GPR143 genes in familial and sporadic cases by sequencing analysis. Based on this screening analysis the molecular diagnosis was carried out especially for carrier detection, those families are under risk condition because of the presence of this diseases in their previous generation.
    Alejandro Acosta, Pedro J. Dávila, and Natalio J. Izquierdo*
    Introduction: The Hermansky-Pudlak syndrome is an autosomal recessive disease characterized by oculo cutaneous albinism, a bleeding diathesis and lysosomal accumulation of ceroid lipofuscin.
    Objectives: To do a comprehensive literature review of the clinicopathological findings in patients with the Hermasnky-Pudlak syndrome, its diagnosis, management, and treatment.
    Methods: A literature review of the Hermansky-Pudlak syndrome was done.
    Conclusion: Patients with the various genotypes leading to the Hermansky-Pudlak syndrome have multiple ocular and systemic manifestations with extensive genotypic and phenotypic variability. Co-management between Primary Physicians, Ophthalmologists, and other sub-specialists is of outmost importance. Patients’ co-management must be customized individually, taking into account patient’s end goal, comorbidities, and bleeding diathesis. Genetic testing and counseling is of outmost importance in patients with the syndrome.
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