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Mutations in some homeotic genes can often be lethal and the cycle of life will end at embryogenesis.
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Mutations and some
Mutations in captivity have emerged in various colors, some quite different from those observed in nature.
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 to the V-ATPase ' a4 ' or ' B1 ' isoforms result in distal renal tubular acidosis, a condition that leads to metabolic acidosis, in some cases with sensorineural deafness.
Mutations in the surface proteins allow the virus to elude some host immunity, and the numbers and locations of these mutations that confer the greatest amount of immune escape has been an important topic of study for over a decade.
Mutations in receptors that result in increased constitutive activity underlie some inherited diseases, such as precocious puberty ( due to mutations in luteinizing hormone receptors ) and hyperthyroidism ( due to mutations in thyroid-stimulating hormone receptors ).
In humans, GABA < sub > A </ sub >- ρ receptor subunits ρ1 and ρ2 are encoded by the and genes which are found on chromosome 6 whereas the gene for ρ3 is found on chromosome 3 Mutations in the ρ1 or ρ2 genes may be responsible for some cases of autosomal recessive retinitis pigmentosa.
Mutations and genes
Mutations in several genes have been linked to several types of epilepsy.
Mutations in two regulatory genes of white grapes turn off production of anthocyanins which are responsible for the color of purple grapes.
Mutations in the genes for the hemoglobin protein in a species result in hemoglobin variants.
Mutations in viral genes weakened their infectious ability, sometimes creating viruses that were able to infect and grow within only certain varieties of E coli.
Mutations in genes can cause also affect skin colour through oculocutaneous albinism ( OCA ) – a lack of pigment in the eyes, skin and sometimes hair that occurs occasionally in a very small fraction of the population.
Mutations / knockout of other genes affecting the GH / IGF1 axis, such as Lit, Ghr and Irs1 have also shown extension in lifespan, but much more modest both in relative and absolute terms.
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 in a number of different genes as well as RAS itself can have this effect.
Mutations in either of two major susceptibility genes, breast cancer susceptibility gene 1 ( BRCA1 ) and breast cancer susceptibility gene 2 ( BRCA2 ), confer a lifetime risk of breast cancer of between 60 and 85 percent and a lifetime risk of ovarian cancer of between 15 and 40 percent.
Mutations in these genes account for 70 to 80 percent of all cases of cerebral cavernous malformations.
Mutations in both copies of the PCCA or PCCB genes cause propionic acidemia.
Mutations in the PCCA or PCCB genes disrupt the function of the enzyme, preventing these acids from being metabolized.
* Mutations that cause CFC are found in the KRAS, BRAF, MEK1 and MEK2 genes.
Polycystic Disease is a genetic disease caused by Mutations in the PKD1, PKD2, and PKHD1 genes.
Mutations in the KCNH2, KCNJ2, and KCNQ1 genes cause short QT syndrome.
Mutations in any of these genes prevent the proper production or assembly of the type IV collagen network, which is an important structural component of basement membranes in the kidney, inner ear, and eye.
Mutations that affect the normal function of these genes can result in retinitis pigmentosa and vision loss.
Mutations in the genes expressing this protein have been associated with the PC1 variant of pachyonychia congenita, an inherited disorder of the epithelial tissues in which keratin 6A is expressed, particularly leading to structural abnormalities of the nails, the epidermis of the palms and soles, and oral epithelia.
Mutations in the genes encoding this protein have been associated with White Sponge Nevus, characterized by oral, esophageal, and anal leukoplakia.
Mutations in the genes for these keratins are associated with epidermolysis bullosa simplex and Dermatopathia pigmentosa reticularis, both of which are autosomal dominant mutations.
Mutations in these genes typically lead to the synthesis of a truncated EXT protein which does not function normally.
Mutations in either of these genes disrupt the ability of this transporter protein to reabsorb these amino acids, allowing them to become concentrated in the urine.
Mutations in the genes that control the formation of down feathers have been recorded in a German White Leghorn flock.
Mutations of the wingless gene in the fruit fly were found in wingless flies, while tumors caused by MMTV were found to have copies of the virus integrated into the genome forcing overproduction of one of several Wnt genes.
Mutations and can
Mutations in the gene for the prion protein can cause a misfolding of the dominantly alpha helical regions into beta pleated sheets.
One deck represents random Alpha Mutations, which can be drawn to gain temporary powers, and the other contains various Omega Tech, powerful technological devices that could possibly backfire on those that use them.
Mutations in the gene HR can lead to complete hair loss, though this is not typical in humans.
Mutations can have an impact on the phenotype of an organism, especially if they occur within the protein coding sequence of a gene.
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 in such microRNAs ( known as oncomirs ) can lead to activation of oncogenes.
Mutations in the androgen receptor gene can cause problems with any of the steps involved in androgenization, from the synthesis of the androgen receptor protein itself, through the transcriptional ability of the dimerized, androgen-AR complex.
* Mutations in the OFD1 gene can also cause several other disorders with features that overlap with those of oral-facial-digital syndrome.
Mutations can be detected in 90 %.
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 these proteins can result in altered functionality of sub-complex assembly, copper transport, or translational regulation.
Mutations of the FOXP3 gene can prevent regulatory T cell development, causing the fatal autoimmune disease IPEX.
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 and natural selection can only " remove preexisting information.
Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.
Mutations in these areas can lead to non-functional proteins that can polymerise and accumulate in the liver ( infantile hepatic cirrhosis ).
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 of the gene for this enzyme can cause unusual forms of diabetes or hypoglycemia.
* SGSH Mutations can cause Sanfilippo syndrome
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