Bioreporters are intact, living microbial cells that have been genetically engineered to produce a measurable signal in response to a specific chemical or physical agent in their environment.
 Bioreporters contain two essential genetic elements, a promoter gene and a reporter gene.
 The promoter gene is turned on (transcribed) when the target agent is present in the cell’s environment.
 The promoter gene in a normal bacterial cell is linked to other genes that are then likewise transcribed and then translated into proteins that help the cell in either combating or adapting to the agent to which it has been exposed.
 In the case of a bioreporter, these genes, or portions thereof, have been removed and replaced with a reporter gene.
 Consequently, turning on the promoter gene now causes the reporter gene to be turned on.
 Activation of the reporter gene leads to production of reporter proteins that ultimately generate some type of a detectable signal.
 Therefore, the presence of a signal indicates that the bioreporter has sensed a particular target agent in its environment.
Don Fullmer (February 21, 1939 – January 28, 2012) was an American professional boxer and a brother of the former world middleweight champion Gene Fullmer.
 Eight years younger than his more famous brother, Don followed Gene into the gym in West Jordan, Utah, to learn how to box.
 He fought as an amateur for four years and did not lose in sixty-five fights.
 Another brother, Jay, was also active in boxing.
Heterologous expression refers to the expression of a gene or part of a gene in a host organism, which does not naturally have this gene or gene fragment.
 Insertion of the gene in the heterologous host is performed by recombinant DNA technology.
 After being inserted in the host, the gene may be integrated into the host DNA causing permanent expression, or not integrated causing transient expression.
 Heterologous expression can be done in many type of host organisms.
 The host organism can be a bacterium, yeast, mammalian cell, or plant cell.
 This host is called the "expression system".
Haploinsufficiency is a mechanism of action to explain a phenotype when a diploid organism has lost one copy of a gene and is left with a single functional copy of that gene.
 Haploinsufficiency is often caused by a loss-of-function mutation, in which having only one copy of the wild-type allele is not sufficient to produce the wild-type phenotype.
 It occurs when an organism has a single functional copy of a gene, and that single copy does not produce enough product to display the wild type's phenotypic characteristics.
 The genotypic state in which one of two copies of a gene is absent is called hemizygosity.
 Hemizygosity is not the same as haploinsufficiency; hemizygosity describes the genotype, and haploinsufficiency is a mechanism that may have caused the phenotype.
 The general assumption is that the single remaining functional copy of the gene cannot provide sufficient gene product (typically a protein) to preserve the wild-type phenotype leading to an altered or even diseased state.
 As such, haploinsuffiency is typically transmitted with dominant inheritance, either autosomally or X-linked in female humans.
Cis AB is a rare mutation in the ABO gene which complicates the basic inheritance pattern and blood-transfusion compatibility matching for ABO blood typing.
 There are different DNA mutations of either type A or Type B alleles that change several amino acids in enzyme transferase A or B, homologous enzymes differing in only four of 354 amino acids (R176G, G235S, L266M, and G268A).
 A single change in ABO gene DNA could reverse type B to type A and then, a new hybrid enzyme will produce both weak B and A2 (in serum test, A2B and A2B3)).
 The most common mutation is an A105 allele variation in exon 7 nucleotide position G803C changing Glycine (type A) to Alanine (type B).
 There are another 8 alleles reported in BGMUT, the most discovered reciently in China and Taiwan.
 In the cis-AB genotype, both antigens are expressed, like in a standard (trans) AB genotype.
 In a traditional AB phenotype, A and B antigenes are inherited separately from the father and mother while a cis-AB allele comes from one parent only.
 In a serum test, cis-AB tests almost the same as a traditional AB, but people with this rare type have problems with blood transfusions.
 Some of them need components like washed red blood cells or autotransfusion of serum and blood.
Familial hemiplegic migraine (FHM) is an autosomal dominant type of hemiplegic migraine that typically includes weakness of half the body which can last for hours, days or weeks.
 It can be accompanied by other symptoms, such as ataxia, coma and paralysis.
 There is clinical overlap in some FHM patients with episodic ataxia type 2 and spinocerebellar ataxia type 6, benign familial infantile epilepsy, and alternating hemiplegia of childhood.
 There are 3 known loci for FHM.
 FHM1, which accounts for approximately 50% of FHM patients, is caused by mutations in a gene coding for the P/Q-type calcium channel α subunit, CACNA1A.
 FHM1 is also associated with cerebellar degeneration.
 FHM2, which accounts for <25% of FHM cases, is caused by mutations in the Na+ /K+ -ATPase gene ATP1A2.
 FHM3 is a rare subtype of FHM and is caused by mutations in a sodium channel α-subunit coding gene, SCN1A.
 These three subtypes do not account for all cases of FHM, suggesting the existence of at least one other locus (FHM4).
 Many of the non-familial cases of hemiplegic migraine (sporadic hemiplegic migraine) are also caused by mutations at these loci.
 A fourth gene that has been associated with this condition is the proline rich transmembrane protein 2 (PRRT2) - an axonal protein associated with the exocytosis complex.
 A fifth gene associated with this condition is SLC4A4 which encodes the electrogenic NaHCO3cotransporter NBCe1.
Kniest Dysplasia is a rare form of dwarfism caused by a mutation in the COL2A1 gene on chromosome 12.
 The COL2A1 gene is responsible for producing type II collagen.
 The mutation of COL2A1 gene leads to abnormal skeletal growth and problems with hearing and vision.
 What characterizes kniest dysplasia from other type II Osteochondrodysplasia is the level of severity and the dumb-bell shape of shortened long tubular bones.
 This condition was first diagnosed by Dr. Wilhelm Kniest in 1952.
 Dr. Kniest noticed that his 50 year old patient was having difficulties with restricted joint mobility.
 The patient had a short stature and was also suffering from blindness.
 Upon analysis of the patient's DNA, Dr. Kniest discovered that a mutation had occurred at a splice site of the COL2A1 gene.
 This condition is very rare and occurs less than 1 in 1,000,000 people.
 Males and females have equal chances of having this condition.
 Currently, there is no cure for kniest dysplasia.
 Alternative names for Kniest Dysplasia can include Kniest Syndrome, Swiss Cheese Cartilage Syndrome, Kniest Chondrodystrophy, or Metatrophic Dwarfism Type II.
The Utah Sports Hall of Fame is an athletics hall of fame in the U.S. state of Utah.
 The Utah Sports Hall of Fame Foundation, organized in 1967 as The Old Time Athletes Association, was founded "to celebrate and preserve Utah's storied sports heritage."
 The charter class of 18 members was inducted in 1970 and included Jack Dempsey, Gene Fullmer, and Frank Christensen.
 Other inductees include professional basketball player Fred Sheffield (1975), Major League Baseball pitcher Kent Peterson (1977), and rodeo champion Earl W. Bascom (1985).
Gene doping is the hypothetical non-therapeutic use of gene therapy by athletes in order to improve their performance in those sporting events which prohibit such applications of genetic modification technology.
 s of April 2015 , there is no evidence that gene doping has been used for athletic performance-enhancement in any sporting events.
 Gene doping would involve the use of gene transfer to increase or decrease gene expression and protein biosynthesis of a specific human protein; this could be done by directly injecting the gene carrier into the person, or by taking cells from the person, transfecting the cells, and administering the cells back to the person.
Lawrence Gene Fullmer (July 21, 1931 – April 27, 2015) was an American middleweight boxer and world champion.

Question: Done Fullmer and Gene Fullmer were both what type of athlete?
Answer: boxer