Since the X chromosome in males alone, all the condition of sex-linked inheritance is due to genes on the same chromosome. In the 1930s it was found that color-blindness and hemophilia in the alike family came together largely in inheritance through females (who sticks his two Xer before egg formation), the plants were so close with each other that they were "genetically linked." The first coupling ratio of autosomes was discovered in 1951 by Jan Mohr (between Lutheran-blood type and secretary vileness). Only when these were shown connected to other inherited characteristics (an enzyme system and a serum protein), in 1983 show that these genes were on chromosome 19 in the same link group found him and later researcher's gene for a dominantly genetic muscular dystrophy myotonic. AB0-blood types were discovered in 1900, and in 1924 realized that there was a single pair of genes that determined the blood group variation. However, it lasted until 1975, before they knew gene locus for AB0 was on chromosome 9. It was an enzyme polymorphism (AK, adenyl kinase) was previously shown connected to the AB0 genes that allowed the mapping of the chromosome. In 1987, a dominant nerve disease (tuberous sclerosis) appended to this linkage group using DNA types.
Mapping of genes of the chromosomes was first recorded in the 1970s because of the hybrid cell technique, accelerated in the 1980s because of recombinant DNA techniques, and exploded in the 1990s because of the numerous micro-satellites (see above) and physical mapping methods. The hybrid technique use's laboratory produced mixed cells from two species, typically human and hamster or human and mouse. These cells have both species' chromosomes, but will gradually lose human chromosomes when they divide. One can then follow the loss of the human enzyme types in parallel with chromosome loss, and to determine how plants are enzymes. From the first mapping of a functional gene to a precise autosome in 1969, the number rose to approx. 250 in 1977 to approx. 600 in 1986. As of 1996, there were well characterized 3700 gene loci (locus is the same as the location for a gene on a chromosome) to their specific locations on chromosomes, of which 1049 had one or more mutations that gave single ticket disease, the other known due to the cloning of genes for proteins or the detection of genes by DNA sequencing (chromosome "walking"). During and after the sequencing of the total human genome (see Human Genome Project), you would think all of Mendelian inherited characteristics were gene identified, but this is far from the case. There is still a good number of cataloged Mendelian diseases or genome - that is evidence of environmental effects.
When a single ticket disease or gene as simple chromosome mapped by family method to a specific location on a chromosome, and also mapped to the same place the gene for a known protein or enzyme, the last a candidate for the disease. One can then look in the gene for a mutation to explain the disease. Through the human genome project, walk a different path, namely a direct DNA sequencing of a larger piece of chromosome, including the detection of coding DNA.
