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How does a trait become genetic?

How does a trait become genetic?


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How does a trait become genetic? If a trait is passed down from parent to offspring how is it made that the trait is passed along as heritable. If a woman is similar to her mother and she is sexually selected on this basis. Would this make the trait become genetic? Parent favors Offspring with traits that they have that are similar to their own selves. Would this make it genetic?


The whole question is based on the assumption that it makes sense to talk about genetic trait, while it is actually a little bit undefined. The closest existing concept you might want to read about is the concept of heritability. Please see my comments in your text and especially the links on heritability.


Evolutionary psychology and genetics how does a trait become genetic

I don't understand why you are talking about evolutionary psychology in your title. The rest of the post seems unrelated.

As you have received a downvote which might be related to your title, I have now edited your title.

How does a trait become genetic?

It is unclear by what you mean here. But you should probably read about the post Why is a heritability coefficient not an index of how “genetic” something is?.

If a trait is passed down from parent to offspring how is it made that the trait is passed along as heritable.

Again, this is unclear. From the above link post, if at least part of the variation for a phenotypic trait is caused by genetic variation, then the trait is heritable (heritability differs from zero). If a trait is heritable, then parents and offspring will tend to look alike (see Why does the slope of parent-offspring regression equal the heritability in the narrow sense?).

If a woman is similar to her mother and she is sexually selected on this basis. Would this make the trait become genetic?

I don't understand why you are talking about sexual selection here.

Note that selection act on population, selecting specific genetic variants. Talking about an individual being selected just mean that the individual is carrying the genetic variant that is associated with higher fitness in the population.

Note also, that without heritability, there is no selection. You should have a look at Lewontin recipe, for example at the post How does Darwinian Evolution work?.

Parent favors Offspring with traits that they have that are similar to their own selves.

Do they? In humans? In other species? It would require a reference to really what process you are referring to and whether it is actually true.

Would this make it genetic?

Again, this is unclear unfortunately.


Genetic Equilibrium

Genetic equilibrium is a term used to describe a condition of static, or unchanging, allele frequencies in a population over time. Typically in a natural population the frequencies of alleles tend to shift as generations pass and different forces act on a population. This could be caused by many factors including natural selection, genetic drift, mutation and others which forcibly change the allele frequency. However, if a population is at genetic equilibrium these forces are absent or cancel each other out. The examples below show genetic equilibrium from a modeling context and in a natural context.


Phenotype and Genetic Variation

Genetic variation can influence the phenotypes seen in a population. Genetic variation describes the gene changes of organisms in a population. These changes may be the result of DNA mutations. Mutations are changes in the gene sequences on DNA. Any change in the gene sequence can change the phenotype expressed in inherited alleles. Gene flow also contributes to genetic variation. When new organisms migrate into a population, new genes are introduced. The introduction of new alleles into the gene pool makes new gene combinations and different phenotypes possible. Different gene combinations are produced during meiosis. In meiosis, homologous chromosomes randomly segregate into different cells. Gene transfer may occur between homologous chromosomes through the process of crossing over. This recombining of genes can produce new phenotypes in a population.


How To Become A Geneticist

research and study the inheritance of traits at the molecular, organism or population level. May evaluate or treat patients with genetic disorders.

Table of contents

To become a Geneticist, you will need a Bachelor’s Degree in Genetics, Biology, Chemistry, or a related field. You can get a job as a researcher once you have a Bachelor’s Degree.

If you want to work in a management or teaching position in Genetics, you will need to go to graduate school to earn a Master’s or Doctorate Degree in Genetics.

In graduate school, you can specialize in the branch of Genetics that is most interesting to you. You can specialize in Ecological Genetics, Medical Genetics, Behavioral Genetics, and more.

Geneticists Requirements

Step 1: Study the Sciences in High School

Genetics is a field of science, so you will want to develop a strong foundation in sciences in high school. You should focus on Biology, Chemistry, and other science classes so that you are prepared for college level courses.

Step 2: Earn a Bachelor’s Degree

If you want to become a Geneticist, you need to earn your Bachelor’s Degree in Genetics, Biology, or Chemistry. You will take a lot of science courses in addition to your General Studies requirements. During this time, you should develop an idea of what branch of Genetics interests you. If you only obtain the Bachelor’s Degree, your employment opportunities are limited to research as a laboratory assistant, and there is very little opportunity for advancement in your career.

You need to decide which brand of Genetics you want to pursue so that you can prepare for graduate school. Your courses will help you learn enough about Genetics to determine which field is most interesting to you. You will take courses such as Zoology, Botany, Biochemistry, Molecular Chemistry, Microbiology, and more. You will need to decide whether you want a career that deals with people, plants, or animals, and you can narrow this down as you advance through college.

Step 3: Earn Your Graduate Degree

The type of graduate degree you pursue is dependent on the type of Geneticist you aspire to become. You can pursue a Master’s Degree, which takes approximately two years. If you earn your Master’s Degree in an accredited program, you can become a Genetics Counselor. You can specialize in prenatal counseling or work with people who have rare genetic disorders.

If you are looking for greater opportunities for career advancement, you will want to earn a PhD or a Medical Degree. If you earn your PhD, you will be able to get a job teaching at a college and heading up a research team. You can specialize in any field of Genetics and pursue your career.

If you are interested in becoming a Medical Geneticist, you will need to go to Medical School. There are two different types of degrees offered by Medical Schools, including the DO and the MD. You can choose either one to become a Geneticist. A DO is a Doctor of Osteopathic Medicine, and it takes a more holistic approach to medicine by considering nutrition, environment, and the body system as a whole. An MD is a Doctor of Medicine, and it is designed to help people improve their health.

Medical Geneticists treat patients who have genetic disorders. They begin Medical School with two years of science and laboratory training. Then, they move to two years of supervised clinical experience in various medical fields. In the fourth year of Medical School, students take a Medical Licensing exam and apply for residency positions.

Step 4: Secure a Residency

Once students complete Medical School, they move on to their residency training. They spend the first two years in a general medical field such as internal medicine, obstetrics and gynecology, or pediatrics. After two years, they can move into a genetics subspecialty.

Clinical Genetics is a primary specialty, and students take the board exam after two years of experience in residency. If you want to specialize further, you can continue training in subspecialties, including molecular genetics, medical biochemical genetics, and more.

Step 5: Become Board Certified

Once you have completed your residency, you can take the board exams offered by the American Board of Medical Genetics and Genomics. You must pass this exam to become certified as a Clinical Geneticist.

Step 6: Maintain Your Certification

You will need to maintain your certification with continuing education courses and seminars. It is important to stay current in the field so that you can provide the latest treatments and tests to your patients.

What degree do most Geneticists have

We did a survey to ask other Geneticists what degree they had when they first became one. Here are the results.


More Information

For an in depth review of the existing research:
Sexual Orientation, Controversy, and Science, Bailey et al 2016



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Genes are not the only thing that determines traits

Regardless of how complex genes are, they do one thing: instruct the body what parts to make and when. Not all genes become specific end products in all cells. A huge impact of what and when to produce happens while we grow up. That is, while our body literary builds itself.

Sounds funny, but your body indeed gets instructions on how to build itself from genes. Do we grow tall? Genes instruct to make more of us. Do we have curly hair? Genes make proteins that curl hair. Do we… wait a minute. Is it indeed like that?

Of course, to grow tall, we need specific genes that are associated with being tall. We know it is true, because taller people, on average, have taller offspring. But, to grow tall, the body also has to have raw materials (obtained through food) and energy (obtained though food, again). So, it’s not only genes that determine our height, but also our environment. In this case, how much food we had during our childhood.

Another example is about melanin again. I love it and not because I have brown eyes. While genes determine its production indirectly, you noticed it also requires sunshine to turn these genes on. If there is no sunshine, you can have as many genes as you like, your skin will stay pale. Unless your skin is darker from nature, in which case your body does not need sunlight to produce melanin in the skin. That is the only difference between people of different skin colors.

Sunlight is among several things that can turn genes on. Other things are temperature, color, smell, drugs, or even a word you hear. So, in essence, while, in this article, I tried to explain how genes determine traits, it is still essential to know that “determine” is a clumsy explanation of what is going on.


Who Employs Them? Where Do They Work?

Geneticists can work in various capacities for many different types of employers, ranging from conducting forensic testing for the purpose of solving crimes, to working in a clinical setting for the purpose of counseling patients who are at risk of inheriting a health condition. Below are examples of where geneticists can work:

• Colleges and universities (for teaching and/or research)

• Private research facilities

• Government departments, such as law enforcement agencies, or policy analysis

• Self-employment, typically as a consultant


Contents

Usually organisms that have a higher rate of reproduction than their competitors have an evolutionary advantage. Consequently, organisms can evolve to become simpler and thus multiply faster and produce more offspring, as they require fewer resources to reproduce. A good example are parasites such as Plasmodium – the parasite responsible for malaria – and mycoplasma these organisms often dispense with traits that are made unnecessary through parasitism on a host. [7]

A lineage can also dispense with complexity when a particular complex trait merely provides no selective advantage in a particular environment. Loss of this trait need not necessarily confer a selective advantage, but may be lost due to the accumulation of mutations if its loss does not confer an immediate selective disadvantage. [8] For example, a parasitic organism may dispense with the synthetic pathway of a metabolite where it can readily scavenge that metabolite from its host. Discarding this synthesis may not necessarily allow the parasite to conserve significant energy or resources and grow faster, but the loss may be fixed in the population through mutation accumulation if no disadvantage is incurred by loss of that pathway. Mutations causing loss of a complex trait occur more often than mutations causing gain of a complex trait. [ citation needed ]

With selection, evolution can also produce more complex organisms. Complexity often arises in the co-evolution of hosts and pathogens, [9] with each side developing ever more sophisticated adaptations, such as the immune system and the many techniques pathogens have developed to evade it. For example, the parasite Trypanosoma brucei, which causes sleeping sickness, has evolved so many copies of its major surface antigen that about 10% of its genome is devoted to different versions of this one gene. This tremendous complexity allows the parasite to constantly change its surface and thus evade the immune system through antigenic variation. [10]

More generally, the growth of complexity may be driven by the co-evolution between an organism and the ecosystem of predators, prey and parasites to which it tries to stay adapted: as any of these become more complex in order to cope better with the diversity of threats offered by the ecosystem formed by the others, the others too will have to adapt by becoming more complex, thus triggering an ongoing evolutionary arms race [9] towards more complexity. [11] This trend may be reinforced by the fact that ecosystems themselves tend to become more complex over time, as species diversity increases, together with the linkages or dependencies between species.

If evolution possessed an active trend toward complexity (orthogenesis), as was widely believed in the 19th century, [12] then we would expect to see an active trend of increase over time in the most common value (the mode) of complexity among organisms. [13]

However, an increase in complexity can also be explained through a passive process. [13] Assuming unbiased random changes of complexity and the existence of a minimum complexity leads to an increase over time of the average complexity of the biosphere. This involves an increase in variance, but the mode does not change. The trend towards the creation of some organisms with higher complexity over time exists, but it involves increasingly small percentages of living things. [4]

In this hypothesis, any appearance of evolution acting with an intrinsic direction towards increasingly complex organisms is a result of people concentrating on the small number of large, complex organisms that inhabit the right-hand tail of the complexity distribution and ignoring simpler and much more common organisms. This passive model predicts that the majority of species are microscopic prokaryotes, which is supported by estimates of 10 6 to 10 9 extant prokaryotes [14] compared to diversity estimates of 10 6 to 3·10 6 for eukaryotes. [15] [16] Consequently, in this view, microscopic life dominates Earth, and large organisms only appear more diverse due to sampling bias.

Genome complexity has generally increased since the beginning of the life on Earth. [17] [18] Some computer models have suggested that the generation of complex organisms is an inescapable feature of evolution. [19] [20] Proteins tend to become more hydrophobic over time, [21] and to have their hydrophobic amino acids more interspersed along the primary sequence. [22] Increases in body size over time are sometimes seen in what is known as Cope's rule. [23]

Recently work in evolution theory has proposed that by relaxing selection pressure, which typically acts to streamline genomes, the complexity of an organism increases by a process called constructive neutral evolution. [24] Since the effective population size in eukaryotes (especially multi-cellular organisms) is much smaller than in prokaryotes, [25] they experience lower selection constraints.

According to this model, new genes are created by non-adaptive processes, such as by random gene duplication. These novel entities, although not required for viability, do give the organism excess capacity that can facilitate the mutational decay of functional subunits. If this decay results in a situation where all of the genes are now required, the organism has been trapped in a new state where the number of genes has increased. This process has been sometimes described as a complexifying ratchet. [26] These supplemental genes can then be co-opted by natural selection by a process called neofunctionalization. In other instances constructive neutral evolution does not promote the creation of new parts, but rather promotes novel interactions between existing players, which then take on new moonlighting roles. [26]

Constructive neutral evolution has also been used to explain how ancient complexes, such as the spliceosome and the ribosome, have gained new subunits over time, how new alternative spliced isoforms of genes arise, how gene scrambling in ciliates evolved, how pervasive pan-RNA editing may have arisen in Trypanosoma brucei, how functional lncRNAs have likely arisen from transcriptional noise, and how even useless protein complexes can persist for millions of years. [24] [27] [26] [28] [29] [30] [31]

The mutational hazard hypothesis is a non-adaptive theory for increased complexity in genomes. [32] The basis of mutational hazard hypothesis is that each mutation for non-coding DNA imposes a fitness cost. [33] Variation in complexity can be described by 2Neu, where Ne is effective population size and u is mutation rate. [34]

In this hypothesis, selection against non-coding DNA can be reduced in three ways: random genetic drift, recombination rate, and mutation rate. [35] As complexity increases from prokaryotes to multicellular eukaryotes, effective population size decreases, subsequently increasing the strength of random genetic drift. [32] This, along with low recombination rate [35] and high mutation rate, [35] allows non-coding DNA to proliferate without being removed by purifying selection. [32]

Accumulation of non-coding DNA in larger genomes can be seen when comparing genome size and genome content across eukaryotic taxa. There is a positive correlation between genome size and noncoding DNA genome content with each group staying within some variation. [32] [33] When comparing variation in complexity in organelles, effective population size is replaced with genetic effective population size (Ng). [34] If looking at silent-site nucleotide diversity, then larger genomes are expected to have less diversity than more compact ones. In plant and animal mitochondria, differences in mutation rate account for the opposite directions in complexity, with plant mitochondria being more complex and animal mitochondria more streamlined. [36]

The mutational hazard hypothesis has been used to at least partially explain expanded genomes in some species. For example, when comparing Volvox cateri to a close relative with a compact genome, Chlamydomonas reinhardtii, the former had less silent-site diversity than the latter in nuclear, mitochondrial, and plastid genomes. [37] However when comparing the plastid genome of Volvox cateri to Volvox africanus, a species in the same genus but with half the plastid genome size, there was high mutation rates in intergenic regions. [38] In Arabiopsis thaliana, the hypothesis was used as a possible explanation for intron loss and compact genome size. When compared to Arabidopsis lyrata, researchers found a higher mutation rate overall and in lost introns (an intron that is no longer transcribed or spliced) compared to conserved introns. [39]

There are expanded genomes in other species that could not be explained by the mutational hazard hypothesis. For example, the expanded mitochondrial genomes of Silene noctiflora and Silene conica have high mutation rates, lower intron lengths, and more non-coding DNA elements compared to others in the same genus, but there was no evidence for long-term low effective population size. [40] The mitochondrial genomes of Citrullus lanatus and Curcurbita pepo differ in several ways. Citrullus lanatus is smaller, has more introns and duplications, while Curcurbita pepo is larger with more chloroplast and short repeated sequences. [41] If RNA editing sites and mutation rate lined up, then Curcurbita pepo would have a lower mutation rate and more RNA editing sites. However the mutation rate is four times higher than Citrullus lanatus and they have a similar number of RNA editing sites. [41] There was also an attempt to use the hypothesis to explain large nuclear genomes of salamanders, but researchers found opposite results than expected, including lower long-term strength of genetic drift. [42]

In the 19th century, some scientists such as Jean-Baptiste Lamarck (1744–1829) and Ray Lankester (1847–1929) believed that nature had an innate striving to become more complex with evolution. This belief may reflect then-current ideas of Hegel (1770–1831) and of Herbert Spencer (1820–1903) which envisaged the universe gradually evolving to a higher, more perfect state.

This view regarded the evolution of parasites from independent organisms to a parasitic species as "devolution" or "degeneration", and contrary to nature. Social theorists have sometimes interpreted this approach metaphorically to decry certain categories of people as "degenerate parasites". Later scientists regarded biological devolution as nonsense rather, lineages become simpler or more complicated according to whatever forms had a selective advantage. [43]

In a 1964 book, The Emergence of Biological Organization, Quastler pioneered a theory of emergence, developing a model of a series of emergences from protobiological systems to prokaryotes without the need to invoke implausible very low probability events. [44]

The evolution of order, manifested as biological complexity, in living systems and the generation of order in certain non-living systems was proposed in 1983 to obey a common fundamental principal called “the Darwinian dynamic”. [45] The Darwinian dynamic was formulated by first considering how microscopic order is generated in simple non-biological systems that are far from thermodynamic equilibrium. Consideration was then extended to short, replicating RNA molecules assumed to be similar to the earliest forms of life in the RNA world. It was shown that the underlying order-generating processes in the non-biological systems and in replicating RNA are basically similar. This approach helped clarify the relationship of thermodynamics to evolution as well as the empirical content of Darwin’s theory.

In 1985 Morowitz [46] noted that the modern era of irreversible thermodynamics ushered in by Lars Onsager in the 1930s showed that systems invariably become ordered under a flow of energy, thus indicating that the existence of life involves no contradiction to the laws of physics.


Scientific journal articles for further reading

Ahmetov II, Egorova ES, Gabdrakhmanova LJ, Fedotovskaya ON. Genes and Athletic Performance: An Update. Med Sport Sci. 201661:41-54. doi: 10.1159/000445240. Epub 2016 Jun 10. Review. PubMed: 27287076.

Ahmetov II, Fedotovskaya ON. Current Progress in Sports Genomics. Adv Clin Chem. 201570:247-314. doi: 10.1016/bs.acc.2015.03.003. Epub 2015 Apr 11. Review. PubMed: 26231489.

Webborn N, Williams A, McNamee M, Bouchard C, Pitsiladis Y, Ahmetov I, Ashley E, Byrne N, Camporesi S, Collins M, Dijkstra P, Eynon N, Fuku N, Garton FC, Hoppe N, Holm S, Kaye J, Klissouras V, Lucia A, Maase K, Moran C, North KN, Pigozzi F, Wang G. Direct-to-consumer genetic testing for predicting sports performance and talent identification: Consensus statement. Br J Sports Med. 2015 Dec49(23):1486-91. doi: 10.1136/bjsports-2015-095343. PubMed: 26582191. Free full-text available from PubMed Central: PMC4680136.

Yan X, Papadimitriou I, Lidor R, Eynon N. Nature versus Nurture in Determining Athletic Ability. Med Sport Sci. 201661:15-28. doi: 10.1159/000445238. Epub 2016 Jun 10. Review. PubMed: 27287074.


What Is the Job Demand for Geneticists?

The government predicts that job demand for geneticists as a whole will see little or no change (-2% to 2%), and that competition for basic research positions will be strong. Growth will likely be driven in part by advances in big data and hyper-computing that allow for analysis of large genetic and ecological datasets. Increased interest in the environment and an expanded focus on the medical aspects of genetics will also open up opportunities for environmental geneticists.


Genes that are located on the same chromosome are called linked genes. Alleles for these genes tend to segregate together during meiosis, unless they are separated by crossing-over.Crossing-over occurs when two homologous chromosomes exchange genetic material during meiosis I. The closer together two genes are on a chromosome, the less likely their alleles will be separated by crossing-over. At the following link, you can watch an animation showing how genes on the same chromosome may be separated by crossing-over:www.biostudio.com/d_%20Meioti. ed%20Genes.htm.

Linkage explains why certain characteristics are frequently inherited together. For example, genes for hair color and eye color are linked, so certain hair and eye colors tend to be inherited together, such as blonde hair with blue eyes and brown hair with brown eyes. What other human traits seem to occur together? Do you think they might be controlled by linked genes?

Sex-Linked Genes

Genes located on the sex chromosomes are called sex-linked genes. Most sex-linked genes are on the X chromosome, because the Y chromosome has relatively few genes. Strictly speaking, genes on the X chromosome are X-linked genes, but the term sex-linked is often used to refer to them.

Mapping Linkage

Linkage can be assessed by determining how often crossing-over occurs between two genes on the same chromosome. Genes on different (nonhomologous) chromosomes are not linked. They assort independently during meiosis, so they have a 50 percent chance of ending up in different gametes. If genes show up in different gametes less than 50 percent of the time (that is, they tend to be inherited together), they are assumed to be on the same (homologous) chromosome. They may be separated by crossing-over, but this is likely to occur less than 50 percent of the time. The lower the frequency of crossing-over, the closer together on the same chromosome the genes are presumed to be. Frequencies of crossing-over can be used to construct a linkage map like the one in Figure below. A linkage map shows the locations of genes on a chromosome.

Linkage Map for the Human X Chromosome. This linkage map shows the locations of several genes on the X chromosome. Some of the genes code for normal proteins. Others code for abnormal proteins that lead to genetic disorders. Which pair of genes would you expect to have a lower frequency of crossing-over: the genes that code for hemophilia A and G6PD deficiency, or the genes that code for protan and Xm?



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