In Cystic fibrosis what chromosome is affected?
155534
It's not a chromosome, just a gene, of the chromosome 7. \nI have the name of the gene somewhere. If nobody knows, I'll come with it tomorrow OK?\nOk, it's the CFTR gene (cystic fibrosis transmembrane conductance regulator).
1018240
none\n\n\nyou start with one pair of homologous chromosomes in prophase I of meiosis I.  at metaphase I, these homologues line up across the metaphase plate, and at anaphase, they seperate so that one homologue goes to one pole, and the other homologue goes to the other pole.  after cytokinesis at the end of telophase I, you have one homologue in each cell...that homologue then goes through meiosis II, and at metaphase II, that homologue lines up at the metaphase plate with each sister chromatid facing each pole, and the chromosome is "pulled apart".  Anaphase II pulls the sister chromatids to each pole, and cytokinesis splits the one cell into two....two cells, each containing one sister chromatid of a homologous pair. (although in some text books this is refered to as a single homologue)
430627
You should probably ask a more specific question, but some general info...\n\nGenetic Screening for Self: DNA is parsed to look for genes that are known to cause or be risk factors for certain diseases.\n\nGenetic Screening before Conceiving: To check for recessive genes that both parents carry that could cause disease in their child.  For example, you have to carry 2 genes of cystic fibrosis to actually develop the disease (one from each parent)  If father and mother each have 1 gene for Cystic Fibrosis, neither will show any sign of it, but their child will have 25% chance of getting the gene from both of them and developing the disease.\n\nI hope this has helped!
325168
I don't, but fyi Down's Syndrome is caused by trans-located chromosomes, a.k.a. non-disjunction.  It's likely there are some parents on Y!A with one.
463778
"The case of a young man with del(2) (p11.2p13) is reported. Accounts of previous cases of deletion of the short arm of chromosome 2 are reviewed. Common features include mental retardation, proportional short stature and weight, dysmorphic facial features (a prominent nose, abnormal ears), and abnormal hands. Growth and developmental delay are present during the postnatal period"\n\nhttp://jmg.bmjjournals.com/cgi/content/abstract/30/7/604
62826
Caused by a terminal deletion of the most distal band of the short arm of chromosome 1, monosomy 1p36 is the most commonly observed terminal chromosomal deletion, occurring in approximately 1 in 5,000 births (Shaffer and Lupski 2000; Heilstedt et al. 2003b). As first described by the Shaffer lab in 13 subjects (Shapira et al. 1997), craniofacial characteristics of this contiguous gene deletion syndrome (CGDS)--so-called because it involves the deletion of multiple adjacent genes on the same chromosome arm--include late-closing, large anterior fontanels (membranous intervals at the intersection of the cranial bones at the crown of the skull), brachycephaly (disproportionate shortness of the head), deep-set eyes, flat nasal bridge, asymmetric ears, and pointed chin. Monosomy 1p36 is also associated with mental retardation, developmental delay, hearing impairment, seizures, growth impairment, and heart defects (Shapira et al. 1997; Slavotinek et al. 1999; Heilstedt et al. 2003a). Over 90 subjects with rearrangements of 1p36 have enrolled in our studies, of which 61 were recently published (Heilstedt et al. 2003a). The deletion sizes in the subjects vary considerably (Wu et al. 1999; Heilstedt et al. 2003a); however, there is some uniformity in the origin of the deletions, with over 60% being maternally derived (Wu et al. 1999; Heilstedt et al. 2003a). Candidate genes have been proposed for some of the individual features of monosomy 1p36, including seizures (Heilstedt et al. 2001) and facial clefting anomalies (Colmenares et al. 2002). \n\nThe Shaffer laboratory has recently identified possible mechanisms for the generation and/or stabilization of terminal deletions of 1p (Ballif et al. 2003; Ballif et al. 2004a; Ballif et al. 2004b; Gajecka et al. 2005). In addition, the Shaffer laboratory has recently demonstrated the use of microarrays--a rapid, sensitive, and high-resolution technology for the detection of many chromosomal anomalies--in the detection of deletions of 1p36 (Yu et al. 2003). \n\n\ncheck this article\n\nShapira SK, McCaskill C, Northrup H, Spikes AS, Elder FF, Sutton VR, Korenberg JR, Greenberg F, Shaffer LG (1997) Chromosome 1p36 deletions: the clinical phenotype and molecular characterization of a common newly delineated syndrome. Am J Hum Genet 61:642-650
123745
There are 3 chromosomal patterns that result in Down syndrome. 1. Trisomy 21 (nondisjunction) is caused by a faulty cell division that results in the baby having three #21 chromosomes instead of two. ... In translocation a part of chromosome #21 breaks off ... division and attaches to another chromosome. The presence of ... the 21st chromosome causes the characteristics of Down syndrome
1068360
dna and genetic coding of chromosomes.
327006
You're trying to say you have a synthetic chromosome. I would check all the experiments for contamination, and check the cells for endogenous expression before jumping to that conclusion. There are a lot of hurdles to leap, as mentioned in the other posts.
238345
B Chromosomes are abnormal chromosomes that differ from the basic structure of normal ones.Also called as Supernumerary chromosomes & accessory chromosomes.They are the additional ones found in some individual populations that reduce their viability(esp.,in plants). eg.Maize.
58471
Chromosomes, either X or Y.
512125
in biology, mutations are changes to the genetic material. 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 processes such as meiosis or hypermutation. mutations can be classified based on the effect on the structure of the genetic material:\n\n1. small scale mutations affecting one or a few nucleotides\na. point mutation: exchange of a single nucleotide for another through translations or transversions\na)i. silent mutations: code for the same amino acid\na)ii. missense mutations: code for a different amino acid; i.e. sickle cell anemia\na)iii. nonsense mutations: code for a stop codon, which can truncate the protein\nb. insertions: add one or more extra nucleotides causing a shift in the reading frame (or frameshift)\nc. deletions: remove one or more nucleotides thus altering the reading frame (or frameshift)\n\n2. large scale mutations in chromosomal structure\na. amplifications or gene duplications: leading to multiple copies of chromosomal regions\nb. deletions of chromosomal regions: leads to loss of the genes coded; deletions in chromosome 5p causes cri-du-chat syndrome, deletions in chromosome 15q results in prader-willi syndrome\nc. translocations: interchange of genetic parts from non-homologous chromosomes thus bringing together separate genes to form functionally distinct fusion genes; translocations in chromosome 21 causes down syndrome \nd. inversions: reversing the orientation of a chromosomal segment thus bringing together separate genes to form functionally distinct fusion genes\n\nto detect small scale mutations affecting one or more nucleotides, a variety of tests can be done which in principle will test either the dna composition or the presence/absence of the gene products.\n\nlarge scale mutations in the chromosomal structures can be detected using karyotyping because the chromosomes with mutations would differ in sizes and shapes when compared to the standard. in general the chromosomes with deletions would be relatively smaller and chromosomes with additions would be relatively bigger than their counterparts, while chromosomes with either inversions and translocations would exhibit bridges and/or rings.
83652
A hereditary disease of the exocrine glands, usually developing during early childhood and affecting mainly the pancreas, respiratory system, and sweat glands. It is characterized by the production of abnormally viscous mucus by the affected glands, usually resulting in chronic respiratory infections and impaired pancreatic function. Also called mucoviscidosis.\n\nCystic Fibrosis At A Glance\n\n*Cystic fibrosis (CF) is one of the most commonserious genetic (inherited) diseases. \n*CF gene is carried by 1/20 persons (in *Caucasianpopulations) and 1 in 400 couples is at risk for having childrenwith CF.\n*CF is characterized by the production of abnormalsecretions leading to mucous build-up.\n*CF mucous build-up can impair the pancreas and,secondarily, the intestine.\n*CF mucous build-up in lungs can impair respiration.\n*Early diagnosis of CF is of great importance.\n*Early and continuing treatment of CF is valuable.\n\nFor more information try:  http://www.cff.org/home/
862829
Gene Allele Description\nB=black, b=brown\nC=color deposition, c= no color deposition\n\nParents cross: BbCc  x  BbCc\nGametes: BC; Bc; bC; bc  x  BC; Bc; bC; bc\n\nF1 Punnnet Square\n\n.........BC....Bc....bC....bc\nBC\n\nBc\n\nbC\n\nbc\n\nthe result of the punnet square is as follow:\n\n9/16 B_C_  Black (color deposition)\n3/16 bbCC  Brown (color deposition)\n3/16 BBcc  Yellow (no color deposition)\n1/16 bbcc   Yellow (no color deposition)\n\nratio: 9:3:4\n\ngene c is epistatic on gene B/b
600873
A Robertsonian translocation in balanced form results in no excess or deficit of genetic material and causes no health difficulties. In unbalanced forms, Robertsonian translocations cause chromosomal deletions or addition and result in syndromes of multiple malformations, including trisomy 13 (Patau syndrome) and trisomy 21 (Down syndrome).
697176
Good question.  Calling something Mendelian implies that it is influenced by ONE AND ONLY ONE GENE.  As far as using the word "trait", very few "traits" are influenced by just one gene (i.e. hair color, eye color, skin color, height etc.)   These things are influenced by many genes and often environmental factors.\n\nNow, when you talk about expression of genes, we think of Mendelian disorders.  There are many many single gene disorders, the most common being CF (cystic fibrosis).  Basically if a mutation is inherited dominantly, one copy of a mutation means the phenotype will ALWAYS BE EXPRESSED based on that one mutated gene.  Recessive of course (like CF), means both copies of a gene must be mutated to express the phenotype.\n\nCompare this to something like type I diabetes.  One mutation in a gene associated with diabetes doesn't guarantee that someone will have this disease.  Nor do 2 mutations, or 3, etc.  The term we use for this is penetrance by the way.  Mendelian inheritance means a penetrance close to 100% (meaning every time the given gene is expressed, a phenotype associated with it will be expressed).
355921
Actually, if two people produce a child with Cystic Fibrosis then they are both carriers of the gene. That means that everytime they reproduce there is a 1 in 4 chance that their offspring will have Cystic Fibrosis. \n\nBasically, it is a genetic matrix. Each parent donates 2 genes to the process. Each parent has one healthy gene and one CF gene. There are four possible genetic combinations when two people with the Cystic Fibrosis gene have a child. \n\nThe child could get one healthy gene from each parent and the child will not develop Cystic Fibrosis. \n\nThe child could receive one healthy gene from his mother and one CF gene from his father and the child will not develop Cystic Fibrosis. \n\nThe child could receive one healthy gene from his father and one CF gene from his mother and the child will not develop Cystic Fibrosis. \n\nThe child could get one CF gene from each parent and the child will develop Cystic Fibrosis. \n\nThere are two important things to remember.\n\nFirst, if the child receives a CF gene from his parents he has the potential of passing that gene on to his children. This is especially true if he were to have a child with a woman who also carries the gene.\n\nSecond, this does not mean that if a couple were to have four children only one would be at risk of having Cystic Fibrosis. The odds start all over with each pregnancy. It's like having a little sack with 3 red marbles and 1 blue marble in it. If you take a marble from the sack and it is red but place the marble back in before you draw again, you have an equal chance of pulling that red marble the second time (just like the first time).