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FOXP2 – A Hormone’ Review

Introduction

FOXP2 is a hormone that has been identified by scientists in living organisms which is responsible for the sounds that they produce. Science has made and is still making discoveries about the systems of living organisms with the effort to find out what causes them to behave in a certain manner. It is usually wondered why certain organisms contain almost similar features yet behave differently. Science is assisting in clearing such imaginations by finding out the make up of different organs that distinguish them from the others. A critical study has been done especially on humans and apes to find out the specific components in them that make them share much of the physical yet differ in character. Even though man is thought to have evolved from an ape, apes are said to have some underdeveloped features that limit them from behaving the way humans do. In this study, the hormone FOXP2 has been identified to be responsible for the various sounds that are produced in animals and humans. The sounds produced are however different because of the kind of amino acids that are used to build up the hormone in the organisms.

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What is FOXP2?

FOXP2 stands for Forkhead box protein P2. It is a hormone that is involved in the regulation of human expression. If this hormone is mutated, it causes a serious language disorder in human beings. Giorgio asserts that, “this hormone is also involved in the development of other tissues such as the lung and gut” (5). He also goes forth to assert that, “FOXP2 directly regulates a large number of downstream target genes (5). For example, it affects the CNTNAP2 gene, a member of the neurexin family. This gene is associated with common forms of language impairments.” The hormone is found in both min human beings and chimpanzees but the difference in their makeup is displayed by two amino acids. These amino acids are responsible for the differences in the kind of speech that is displayed by chimpanzees and human beings (Giorgio 3). A study was carried out to find out how the difference in the amino acids impacts the two species. In this study, the neuronal models of the mice and the humans were used and the results suggested that the functions of FOXP2 were affected by the neuronal changes.

What is the function of FOXP2?

There are several functions that are played by this hormone in different organisms. Carmignoto’s described the function of FOXP2 as, the hormone which is necessary for enabling the proper growth of the lungs and the brain. According to him, the hormone is redirected to the tissues of the brain and the lung where it is involved in the mechanical process that will ensure that the brain adequately matures. This implies that a deficiency of this hormone will make an organism not behave as it is supposed to. Studies that have been carried out in mice reveal that mice with no functional copies of FOXP2 display abnormalities in brain regions and die 21 days after birth from inadequate lung development” (4). This is basically because the mice may not be able to integrate the environmental factors and thus not be able to survive. The brain and the lungs are important in coordinating essential body activities that include the intake of oxygen, excretion and the likes. A mouse that is deficient in this hormone that has to assist in the coordination of such activities will therefore perish a few days after its birth. Another function of FOXP2 is the regulation of neuroplasticity in songbirds. The sound that is produced by the songbirds is due to the influence of the hormone on the brain that causes an urge within them to produce the sound. The young zebras have also been identified to benefit from FOXP2 which enables them to produce the sound that they usually produce. The level of FOXP2 in adult organism sdi9fferes from those that are still young, the sound produced may also differ according to the environment and the association thereof. For instances a male zebra will produce a significantly lower sound when singing to a female counterpart compared to other species. The same has also been observed in adult canaries.

There several evidences that FOXP2 is involved in human speech, it is however very reserved min human and takes a critical study for its location and existence to be established. Apart from the above mentioned organisms, the hormone has also been identified in birds and reptiles. However, it is not well conserved in non-human mammals. Even though the hormone is referred to by the same name in all living organisms, there has been a recorded difference min the number of amino acids in those organisms that make their sounds different. In relation to the amino acids that form the hormone in humans, the difference in chimpanzees are two amino acids, in mice, the difference is three amino acids and finally min zebras the difference is seven (Gathercole 24). Sherron indicates that, “some researchers argue that this difference in amino acids between the human beings and the chimps is what has led to the evolution of language in human beings” (462). Some further argue that this close difference in FOXP2 hormone is what has made the chimps closer to human beings than any other animal even in character.

Evidence that FOXP2 is involved in human speech

The investigation was carried out on the KE family revealed that the FOXP2 hormone may be the reason for some language disorders that have been experienced in the family for generations). It had been identified that the problem had been in the family for approximately three generations. An experiment was therefore done on the family members that were affected and those that did not display the abnormality to find out the exact thing that was responsible for it. From this investigation, the family revealed a disorder called autosomal dominant. Sherron indicated that, “In this research, a scan was carried out on the genome of the affected and some of the unaffected family members” (456). The first scan limited the affected space on chromosome which the group called SPCHI. To facilitate the success of the experiment, a chromosome clone that was bacteria in nature was used. As a control experiment, another person with a similar disorder was used who was unrelated to the family. After further research and investigations, this gene was called FOXP2.

Language is unique to humans. According to Carmignoto, “human beings should be explored. This is important so as to understand how human brains uniquely combine to produce infinite meaning (9). Another component of language is vocal learning. This is the ability to modify innate vocalizations to unique new sounds. Vocal learners are animals with this ability. Human speech and birdsong are good examples of vocal learning. This two have provided molecular and physiological evidence. Rodents are not thought to learn their vocalizations. However, the recent discoveries that male mice produce song like sounds raise the question of whether such songs are learnt (Watkins 456).

According to Wolfgang, “the complexity of language and the variety of speech and language disorders affects only one in every twenty children (869).” There is a strong association between mutations and language deficits. Fisher gave the first link between FOXP2 and language (98). As Fishers asserts, “Following investigations carried out on the KE family, the affected members of the family were found to have a heterozygous point mutation, which produced an amino acid substitution, R553H in the DNA- binding domain of the FOXP2 protein (99).” However, Fisher’s discovery gives little understanding of how FOXP2 influences the brain. More scientists have tried to explain this condition, which they associate the FOXP2 protein with behavioral and neuro-imagining studies of a single mutation, the R553H, found in the KE family.

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According to Wolfgang, “despite of the ethical and practical limitations of human studies, analysis of FOXP2 function using human neuro-like cells grown in the laboratory can be highly informative” (870). They can help in assessing disturbances in sub cellular localization. For instance, Fisher indicated that, “the Fisher’s laboratory has each used chromatin immuno-precipitation to isolate fragments of DNA that are directly bound by FOXP2 protein in living neurons” (100). This has allowed the successful isolation of downstream targets (Gathecole 154). According to Gathecole “the FOXP2 gene is implicated in the development of human speech and language and a comparison of the human and chimpanzee FOXP2 protein highlights the differences in function in the two species” (156).

FOXP2 and the Evolution of Language

The KE family was the basis of language impairment study. This family experienced severe difficulty in speaking. This disorder is associated with a mutation in a single autosomal dominant gene linked to a single genetic defect.

From the result soft the test, it was identified that the disorder is not grammar or speech specified. The symptoms that were displayed by the affected family members revealed that they were unable to construct sentences and speak them according to the rules of grammar, thy also had a difficult in coordinating the lips and the mouth for them to speak the words correctly. This condition also affected the IQ of the victims both in the verbal and non-verbal domain. From the findings, it was concluded that this condition was caused by a single gene trait. This gene was found to have a fork head binding, known as the Helix domain. The genes that contain this particular domain are called the FOX genes; the name was however modified to FOXP2 in accordance with nomenclature. Therefore, the problem in speech was a result of the nature of the gene. This shows that FOXP2 has the ability to affect the expression of a large number of genes. The problem of speech that is displayed in children as they grow up was identified to have begun in the embryo. This is the time when the embryo adapts some of the physical and mental characteristics of the parent which determine the character that they will display. There are a number of mutations that occur in the embryo of which will affects the development of the fetus. The mutation of the FOXP2 hormone has been identified to be the reason that affects the latter speech of the humans as they grow.

A study from Enard shows that FOXP2 IS highly conserved. In all cases investigated, the amino acid mutated in the KE family was identical. According to Enard, “this gene is 715 amino acids long and it is identical with no differences in chimpanzee, gorilla and the rhesus monkey” (868). Comparing the occurrence of the hormone min mouse in comparison to other apes, it was found that the amino acids in monkeys differed by one. Comparing the same with gorillas and chimpanzees, they were deficient in two amino acids (Enard 870). According to Enard, “estimates of the mutations in the FOXP2 in the human lineage occurs over 100,000 years ago and it is suspected that these mutations are responsible for the development of human speech and brain” (872).

To sum it up, many reports of FOXP2 claim that it is a gene of language. The development of language is not entirely based on a single mutation in FOXP2. There are many other factors that affect speech, this includes the larynx which affects human beings and makes them to choke food. As Giorgio asserts, the nasal cavity is able to close and hinder the vowels from being nasalized (15).

What would happen if the human gene was expressed in chimps?

According to Fisher, “the human genome carries many genes that have no known function in humans but are functional in animals, for example, human being carry the gene for the mouse tail but the cells in the human being miss the switch to turn it on” (78). This means that adding more mouse tail genes to the human body would not do anything new. Genetic materials are usually carried out across several species which may generally affect their genetic make up. It will make them to display characters that may have been thought to have gone with the previous generation. “Analyses show that these viruses have been frequent visitors throughout generations” (Motoo 718).

Many scientists have tried to develop chimeras in the laboratory but these chimeras do not survive to term (Giorgio 8). The genome that makes up the human character and that which is responsible for the same in chimpanzees has been studied and identified in full. It is therefore easy for scientists to draw a distinction on the characters that are displayed by humans and those displayed by chimpanzees.. Moving from paper to life would require embryonic technologies. Brain-expressed genes are known to evolve slowly in mammals. This means that the rate of evolution among brain expressed genes is low. In addition, evolution is less pronounced in brain specific genes making the human brain differ from that of his close relatives. According to (Kimura 716), coding for the brain is complex and highly constrained. He argues that too much change would impair brain activity. From his studies, he found out that interfering with the chimpanzee genome was likely to produce additional characteristics similar to those of the human being. Morally, the development of chimeras has being opposed by society. Religiously, trying to give chimpanzee human characteristics is interfering with creation which is meant to be sacred.

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There have been efforts by scientist to try and mix up the genome of the chimpanzee and that of the human being to see if the characters can merge. A chimpanzee has been the target of these studies considering the many characters that it shares with the humans. Thy have been hence trying to put the speech hormones in chimpanzees to see if they would make them talk. This has however been in vain considering that the mechanical make up of a chimpanzee can not be compared to that of a human being. The exchange of such materials has been in fact identified to interfere with the make up of the two organisms. The FOXP2 hormone operates mainly in the brain and the lungs, this are crucial organs that can affect the functioning of the body if correct measures are not followed. Scientists have not given up on the study and they do believe that one day they will manage to integrate these hormones to achieve the desired results. FOXP2 hormone is a simple hormone that is composed of different features; the hormone may not remain to be the same because it is transferred from one organism to another. It has continued to display different natures in varying living organisms which is making nit complicated for the scientists to modify it. It is also not easy to obtain especially in humans considering the areas in which they are synthesized and produced.

In conclusion, the FOXP2 protein is responsible for human speech and cognitive development. If this gene was expressed in chimpanzees, it is not a guarantee that the chimps would talk and act like the human beings. This is demonstrated by the fact that human beings carry the mouse tail gene but do not express it physically. Similarly, increasing FOXP2 in chimps does not mean they would talk. Consequently, tampering with brain genes would only result in damage even to a point of ruining the cognitive capacity of chimps. It is not FOXP2 as a single gene that affects speech, but it’s the nature of combination with other cells, which is only unique in the human brain and not in the chimp’s brain. Efforts of producing human speech in a chimpanzee would just be futile (Giorgio 15). Mixing individuals violates their genetic uniqueness thus speech should be left as a unique quality of human beings only. This discovery could be in opposition to the theory of revolution where by man has been thought to originate from apes. Science itself has come up with findings that may reveal that the human genes and those of the apes may not be integrated. The few experiments that have been done have produced negative results that have diverse effects on the victims. In fact apes are rarely used to experiment the appropriate medicine that can be used in humans. Organisms that are mostly used for the same are mice which have revealed more promising results. The journey is however never final for the scientists who are forever behind their microscopes to feed the world with new findings.

Works Cited

Fisher, Gary. Accelerated evolution of nervous system genes in the origin of Homosapiens. New York: Atheneum publishers, 1998.

Gathercole, Susan. Phonological memory deficits in language Columbus. USA: Battelle Institute, 1990.

Giorgio, Carmignoto. What makes man different from other primates? Journal of Physiology, 559 (2006): 3-15.

Motoo, Kimura. On the probability of fixation of mutant genes in a population. Genetics 47 (1999): 713–719.

Sherron, Watkins. Behavioral analysis of an inherited speech and language disorder. Journal of psychology, 125 (2002): 452–464.

Wolfgang, Enard. Molecular evolution of FOXP2, a gene involved in speech and language. Genetics, 418 (2002): 869 – 872.

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