Mutations in two regulatory genes of white grapes turn off production of anthocyanins which are responsible for the color of purple grapes.

Mutations are changes in the DNA sequence of a cell's genome and are caused by radiation, viruses, transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication.

Mutations are caused by radiation, viruses, transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication.

Mutations in transpeptidases that lead to reduced interactions with an antibiotic are a significant source of emerging antibiotic resistance.

Mutations are an important force driving evolution.

Mutations that affect insulin-like signaling in worms, flies, and the growth hormone / IGF1 axis in mice are associated with extended lifespan.

Mutations are permanent, transmissible changes to the genetic material ( usually DNA or RNA ) of a cell.

Mutations are considered the driving force of evolution, where less favorable ( or deleterious ) mutations are removed from the gene pool by natural selection, while more favorable ( or beneficial ) ones tend to accumulate.

Mutations leading to the loss of function of a gene are much more common than mutations that produce a new, fully functional gene.

Mutations in the tafazzin gene ( TAZ, also called G4. 5 ) are closely associated with

Mutations periodically occur within the Y chromosome and these mutations are passed on to males in subsequent generations.

Mutations of the genes VHL, RET, NF1 ( Gene 17 Neurofibromatosis type 1 ), SDHB and SDHD are all known to cause familial pheochromocytoma / extra-adrenal paraganglioma.

Mutations are characterized as either β < sup > o </ sup > or β thalassemia major if they prevent any formation of β chains, the most severe form of β thalassemia.

Mutations are likely to be rare and most mutations are neutral or deleterious, but in some instances the new alleles can be favored by natural selection.

Mutations in the Ras family of proto-oncogenes ( comprising H-Ras, N-Ras and K-Ras ) are very common, being found in 20 % to 30 % of all human tumours.

Mutations in this gene are rare.

Mutations affecting repressor are said to be recessive to wild type ( and that wild type is dominant ), and this is explained by the fact that repressor is a small protein which can diffuse in the cell.

Mutations usually sound at pitches in the harmonic series of the fundamental and, except where they are derived from unit ranks, are always tuned pure.

Mutations within the desmosome are the main cause of Arrhythmogenic right ventricular cardiomyopathy ( ARVC ).

Mutations of the WT1 gene on chromosome 11 p 13 are observed in approximately 20 % of Wilms ' tumors .< ref > At least half of the Wilms ' tumors with mutations in WT1 also carry mutations in CTNNB1, the gene encoding the proto-oncogene beta-catenin.

Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.

Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.

Mutations can be caused by copying errors in the genetic material during cell division and by exposure to radiation, chemicals, or viruses, or can occur deliberately under cellular control during the processes such as meiosis or hypermutation.

Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.

Mutations leading to carcinoma may be accelerated by genetic or environmental factors and other risk factors already described.

Mutations associated with the gene may result in changes in serotonin transporter function, and experiments with mice have identified more the 50 different phenotypic changes as a result of genetic variation.

Polycystic Disease is a genetic disease caused by Mutations in the PKD1, PKD2, and PKHD1 genes.

Mutations are permanent, transmissible changes to the genetic material ( usually DNA or RNA ) of a cell.

Mutations in the gene encoding this protein are associated with the genetic skin disorders pachyonychia congenita, non-epidermolytic palmoplantar keratoderma and unilateral palmoplantar verrucous nevus.

Mutations in the ceruloplasmin gene (< i > CP </ i >), which are very rare, can lead to the genetic disease aceruloplasminemia, characterized by hyperferritinemia with iron overload.

Mutations induced by EMS can then be studied in genetic screens or other assays.

Mutations can have an impact on the phenotype of an organism, especially if they occur within the protein coding sequence of a gene.

Suddenly, evolutionary theorists could answer the charge that spontaneous random mutations should result overwhelmingly in deleterious changes to a fragile, monolithic genome: Mutations in homeobox regulation could safely — yet dramatically — alter morphology at a high level, without damaging coding for specific organs or tissues.

Mutations in this region can affect rate of efficiency of gene transcription, which in turn can alter levels of mRNA and, thus, protein levels in general.

Mutations in the SLC26A2 gene alter the structure of developing cartilage, preventing bones from forming properly and resulting in the skeletal problems characteristic of diastrophic dysplasia.

Mutations in these genes alter the usual structure and function of potassium channels or prevent the assembly of normal channels.

Mutations in any of these genes alter the structure or function of channels, which changes the flow of ions between cells.

Mutations in the KCNJ2 gene alter the usual structure and function of potassium channels or prevent the channels from being inserted correctly into the cell membrane.

Mutations in SLC25A13 typically prevent the production of any functional citrin, which inhibits the urea cycle and disrupts the production of proteins and nucleotides.

Mutations of mitochondrial DNA can lead to a number of illnesses including exercise intolerance and Kearns-Sayre syndrome ( KSS ), which causes a person to lose full function of heart, eye, and muscle movements.

Mutations in the DNA binding regions for either of these proteins results in ablation of transgene GLUT-4 expression.

Mutations generally occur in the DNA encoding the intracellular part ( exon 11 ), which acts as a tyrosine kinase to activate other enzymes.

Mutations in the BLM gene, which is a member of the RecQ DNA helicase family, are associated with Bloom syndrome.

Mutations in DNA that lead to cancer ( only certain mutations can lead to cancer and the majority of potential mutations will have no bearing ) disrupt these orderly processes by disrupting the programming regulating the processes.

Mutations in the DNA glycosylase MYH are also known to increase susceptibility to colon cancer.