Each human being has something called DNA. DNA is described as genetics and an extremely long macromolecule that is the main component of chromosomes and is the material that transfers genetic characteristics in all life forms. DNA constructs of two nucleotide strands coiled around each other in a ladder like arrangement with the sidepieces composed of alternating phosphate and deoxyribose units and the rungs composed of the purine and pyrimidine bases adenine, guanine, cytosine, and thymine. Each chromosome consist of one continuous thread-like molecule of DNA coiled tightly around proteins and contains a portion of the 6,400,000,000 basepairs that make up your DNA.
Epigenetics can be hereditable or environmental factors that affect the expression of genes and lead to changes in gene expression. Unlike genetics, epigenetics does not only have to do with which genes are passed down to the offspring and the DNA sequence. The environmental conditions of the offspring’s parents impact the genes in their eggs and sperms by “switching on” certain genes and “switching of” others (Dowshen). Since the genes expression of the gametes are affect, the phenotypes of the offspring will change. Even in a person’s lifetime, environmental factors such as stress, chemical exposure, and diet can continue to impact gene expression through DNA methylation. During DNA methylation, a methyl group is randomly added to a 5-carbon cytosine ring, making 5-methylcytosine and these groups inhibit transcription. (Cheriyedath). Due the fact that transcription is not possible, the expressing of the genes in that section of the DNA strand will be suppressed. The attachment of the methyl group to DNA is not determined, which means that
The article that I found discusses how DNA evidence was used to convict a suspect after twenty years under investigation. The homicide case was recently closed on the rape and murder of Ophelia Preston, a 24 year-old female in Milwaukee County. Preston was deaf and mute and also suffered from a cocaine addiction, which led her to meeting Melvin Lee Jones.
Cancer is a disease caused by an uncontrolled division of abnormal cells. The DNA sequence in cells can be changed as a result of copying errors during replication. If these changes whatever their cause are left uncorrected, both growing and non-growing somatic cells might gain many mutations that they could no longer function. The relevance of DNA damage and repair to the generation of cancer was obvious when it was recognized that everything that causes cancer also cause a change in the DNA sequence. Tumor suppressor genes are protective genes and normally they limit cell growth by monitoring the speed of cell division, repair mismatched DNA and control when a cell dies. When a tumor suppressor gene is mutated cells grow
On December 10, 2015, three profound individuals received the Nobel Prize in chemistry for their work on DNA repair systems. Paul Modrich, Thomas Lindahl, and Aziz Sancar studied how the cell repairs and protects the information held in its DNA; specifically, Paul Modrich focused on DNA mismatch repair. Since DNA constantly replicates, damage and incorrect pairings are expected, but enzymes watch over DNA as it replicates and repair any errors that occur. In the mismatch repair system, enzymes find the mismatch in the copy of DNA, cut the incorrect section out, and replace it with the correct sequence. Paul Modrich’s study of the mismatch repair system has provided the medical field with important information regarding cancer growth and the possibility of a cure.
possible error allowing repair thus achieving high fidelity in transcription. Also, the DNA damage response system can activate checkpoints inducing cell cycle arrest, allowing time for different mechanisms such as Base, Nucleotide Excision Repair and Mismatch Repair system which, involving specialized proteins, will excise and repair the incurred error.
On September 12, 1016, Belmont University graciously allowed Dr. Katherine Friedman from Vanderbilt University to come and talk to a crowd of students about the tendencies of how deoxyribose double stranded breaks can during cell replication and the elements required to hopefully repair this ordeal. She began the session by discussing what chromosomes are composed of and how they are produced, accompanied by visual and statistical representations. Moving on, she touched on how double strand breaks are a huge threat to a cell's, an organisms, stability. Correspondingly, she described what can cause these breaks; chemical factors, as well as inner cell disruptions during replication that are sometimes hard to remedy. However, she also stated that this breaks can occur on purpose, mostly in the immune system in efforts to make antibodies.
The gene that we are interested in for this project and for the duration of this semester is DMAP1. Not a lot is known about this is a gene, however in other organisms, it is involved in the methylation of DNA. DMAP1 is responsible for encoding a protein that associates with another protein that methylates DNA. The methylation of DNA alters the DNA structure and makes it unavailable to transcription factors, so the mutation of DMAP1 could lead to changes in transcription and gene regulation. For example, if DMAP1 were mutated, less DNA methylation might occur and more areas of DNA could be accessible to transcription factors and ‘active’, making more genes transcribed than should be. Gene alterations are important as they can lead
Methylation, specifically hypomethylation, can incessantly activate the transcription of oncogenic microRNAs which encourage carcinogenesis (Fukushige). Methylation, specifically hypermethylation, of the genome can turn off genes that can be transcripts to make microRNAs which actively work to suppress tumors. When a microRNA suffers from mutations, the altered miRNA can promote hypermethylation of tumor-suppressor genes (Lopez). DNA methylation affects the regulation of harmful, cancer-causing and can increase the incidence of pancreatic cancer. Cancer tissues were shown to have extraordinarily higher levels of methylation than non-cancerous tissues did
The study greatly helped in understanding the mechanism of nutrition and epigenetic inheritance to the child while in the womb. It has been shown through animal studies that a methyl rich diet of the mother gives a progeny with a highly methylated DNA. Specifically, studies in mice have shown that diet affects the Agouti gene (present in all mammals) when the gene is not methylated the mice shows a yellow coat, a fatter complexion and is likely to develop diabetes and cancer. Unlike the healthy mice
Since the DNA structure was discovered more than 50 years ago, the mechanisms how genetic information encoded by DNA was preserved and how the integrity of transmission in between generations was maintained have been one of the top questions kept being asked. It has been well accepted that the integrity of human genome is maintained by mechanisms to protect DNA from damage either generated spontaneously during endogenous DNA biogenesis including replication or transcription or induced by exogenous environmental factors (Ciccia and Elledge, 2010; Jackson and Bartek, 2009; Lord and Ashworth, 2012).
Before HITI, recent techniques in the area of gene-editing were focused on using a natural DNA repair pathway, called homology-directed repair (HDR). These systems are targeted at dividing cells, such as the skin, but has been proven to be ineffective in nondividing cells, and therefore inefficient to provide solutions to genetic disorders in adult tissue. However, the non-homologous end-joining (NHEJ) pathway is an additional natural DNA repair pathway, which is typically unused in gene insertion, as studies have shown that NHEJ is “error prone when used to turn off targeted genes” (…). Yet, when used in insertion of DNA sequences in a gene, NHEJ is highly precise, and more
Two sample proteins from yeast were used to study the response of DNA binding proteins to nucleosomes along DNA. Theses protein complexes are mlhs1-pms1 and msh2-msh6 (Gorman, Plys et al. 2010). Though both used in mismatch repair, the two complexes function differently. Msh2-msh6 mainly repairs single base pairs (Kunkel et al. 2005). In addition, it is also often used to initiate repair by binding to DNA. Mlh1-pms1, instead of repairing just a few bases pairs, repairs a much longer strand of up to sixteen nucleotides.
Modification of damaged DNA seems to be an understudied subject, there is much to understand on the restoration of DNA damage, repair and DNA methylation. Genomic DNA can be modified by methylation but much of it is affected on a gene when silenced. When epigenetic modification has been implicated with cancer and aging it causes DNA methylation to also have an impact on the double strand of DNA analysis. Modification as such provoke deteriorating changes like aging found in multicellular organisms and DNA damage may magnify biochemical pathways that regulate a cells growth or control DNA replication with DNA repair. In the article “DNA Damage, Homology-Directed Repair, and DNA Methylation” written by Concetta Cuozzo, Antonio Porcellini, Tiziana Angrisano, et al. they hypothesize how DNA damage and gene silencing may induce a DNA double-strand break within a genome as well as when DNA methylation is induced by homologous recombination that it may somewhat mark its reparation through a DNA segment and protect its cells against any unregulated gene expression that may be followed by DNA damage. The experiments used to demonstration how gene conversion can modify methylation pattern of repaired DNA and when that occurs methylation is able to silence the recombined gene. When exploring the molecular mechanisms that link DNA damage and the silencing gene then there is an induced double strand break that can be found at a specific location or DNA sequence in where the