an unknown base triplet is missing from the gene for the height of an animal?
448280
DNA from organisms displaying both normal and abnormal phenotypes. Mutation studies can be done, comparing the sequences of normal and abnormal, isolating the gene in question and identifying the protein it encodes. "Knock-out" experiments can also be done, wherein the effect of deleted genes will be observed. Other things to consider would be promoters, suppressors and regulators of the gene.
977253
http://rds.yahoo.com/_ylt=A0geurcTqmtFzHYATAJXNyoA;_ylu=X3oDMTE2OWZqMTJjBGNvbG8DZQRsA1dTMQRwb3MDNQRzZWMDc3IEdnRpZANERlI1Xzgz/SIG=12nmp8dcs/EXP=1164770195/**http%3a//www.pubmedcentral.nih.gov/articlerender.fcgi%3fartid=1371053\n\nhttp://www.vetpathology.org/cgi/content/full/39/5/602\n\nfrom what I am seeing, it can appear in either sex, but has been documented more in heifers. It can be congenital, but does not appear to be sex-linked.
876744
go www.learn.genetic.com i hope u can slove ur problem.
842615
Your question requires more knowledge of science and genetics than I have.  However, since you haven't received much help with it I thought I would give you a couple of sites.  Try these - they may be of some help to you.  Sorry I couldn't help more.
1058758
In the human genome, humans have a base height that is added to the height genes. so if both parents have half tall genes and half short genes (lets just say T for tall and t for short), like the mother may have TtTTtt and the father may have ttTtTT, the the child may turn out many ways, for example it could receive all three tall genes from the mother and all three tall genes from the father (TTTTTT) or it could receive all three short genes from the mother and all three short genes from the father (tttttt) or it could be any combination in-between.(TTtTtT, TTtTTT, TtttTt,...).  However, if both the parents are have all short genes (both have tttttt) then the only combination possible for the child is tttttt, and the same goes for the tall genes.  There is one more major possibility, but the parents would not be the same height.  If the mother had all short genes (tttttt) and the father had all tall genes (TTTTTT) then the child would have 3 short genes and 3 tall genes (TtTtTt not necessarily in that order).  Also keep in mind that there are more than 6 genes that control height.  And just to screw things all up, height depends on more that genetics (environment, eating habits, sports, injuries...).  To make things more complicated, other genes indirectly affect height.
273418
First off, it's only the number of _cervical_ (neck) vertebrae of mammals that is fixed at 7, not all the other vertebral types. There are exceptions, such as the tree sloths with 6 or 9 vertebrae, and a manatee species with 6, but the number 7 is consistent in most species of mammals, from giraffes (although there was an interesting question about it here) to dwarf shrews. \n\nA recent hypothesis (1999) about the fixed nº of cervical vertebrae is related to evolutionary developmental (evo-devo) aspects. Apparently, in mammals the genes that regulate the development of the skeleton (Hox genes) are also linked to the proliferation of cell lines (which is in turn related to the origin of cancer). Thus, any change in the nº of vertebrae could bring about deletereous (negative) changes in the control of cell multiplication, and would be constrained by natural selection because although the fixed nº of cervical vertebrae is not particularly advantageous, the possibility of tumor development is decidedly disadvantageous.\n\nAnd with respect to canislupus' question: If there is such a constraint, maybe the different number of cervical vertebrae in sloths and manatees gives advantages that offset the potential problems. In the case of sloths, I can easily see that more vertebrae enable greater rotation angle of the head (these animals are very impressive when they move). In the case of manatees, I cannot think of an evident advantage, but then again, I don't know much about manatees.\nSee the article at the first link.\n\n------------\nUpdate: I've checked other sources and it appears that both manatees and sloths share one trait: low basal metabolism. This could allow changes in the regulatory Hox gene without the threat of cancer (see second link)\n------------\nUpdate 2: Canislupus, this is new knowledge for me too. That's why I like Answers :-)
100809
They are part of a set of triplets :-)
1001272
no becuase the combinations of the genes
689348
Genetics, diet and exercise or lack thereof.
762553
gene is the DNA or RNA in animals cell
268676
There are actually duplicate genes for every function. You received one from your mother and one from your father. If one is missing or defective, the other takes over. Sometimes both are required and you would express a recessive trait. If the gene is crucial, your life is shortened or aborted.  Some conditions have an entire chromosome missing (Turners syndrome) without catestrophic effects.
659200
I'm not sure what you are asking because of the typos. But here goes an answer for what I think you are trying to ask.\n\nA point mutation involving the addition of a BASE early in the coding, The protein resulting from The gene will be entirely different from the point of addition, since the reading frame will be moved forward. \n\nExample (HYPOTHETICAL)\n\nNormal DNA\nATCGGTACCATT\n\nNormal mRNA\nUAGCCAUGGUAA  The reading frame would be UAG-CCA-UGG-UAA...\n\nmutated mRNA (a C added by mistake)\nUAGCCCAUGGUAA The reading frame would be UAG-CCC-AUG-GUA..\n\nThis can cause the protein to be shorter, because it can create a stop codon somewhere with the addition, also it can make it longer, a stop codon no longer present where it should be.\n\nBasically the protein would be non-functioning.
1069568
Ligers and Tigons are sterile from birth, so there would be no offspring.  However, if one were to unlock the secrets behind genetic recombination, you could sample DNA from both animals and possbly splice a new, third hybrid ... perhaps a Tigron.  Sadly, natural pathways for an enhanced hybrid from these two creatures is impossible.
496136
Not that I'm aware of. This genetic condition involves the X and Y chromosomes, and not anything else.
392240
they have a gene that causes them not to be hairy
762040
Achondroplasia is inherited by an autosomal dominant gene that causes abnormal cartilage formation. Autosomal dominant inheritance means that the gene is located on one of the autosomes (chromosome pairs 1 through 22). This means that males and females are equally affected. Dominant means that only one gene is necessary to have the trait. When a parent has a dominant trait, there is a 50 percent chance that any child they have will also inherit the trait. So, in some cases, the child inherits the achondroplasia from a parent with achondroplasia. The majority of achondroplasia cases (80 percent), however, are the result of a new mutation in the family - the parents are of average height and do not have the abnormal gene.\n\nAs mentioned, persons with achondroplasia have a 50 percent chance to pass the gene to a child, resulting in the condition. If both parents have achondroplasia, with each pregnancy, there is a 50 percent chance to have a child with achondroplasia, a 25 percent chance that the child will not inherit the gene and be of average height, and a 25 percent chance that the child will inherit one abnormal gene from each parent, which can lead to severe skeletal problems that often result in early death.\n\nGeneticists have found that fathers who are older than 45 have a higher chance of having children with certain autosomal dominant conditions such as achondroplasia, but no cause for the new mutations in sperm has been discovered at this time.\n\nThe gene responsible for achondroplasia was discovered in 1994 making accurate prenatal diagnosis available, in most cases.
829110
triplet codons of nucleic bases - adenine, uracil, guanine and cytosine. these form amino acids