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From Wikipedia, the free encyclopedia

Heredity, also called inheritance or biological inheritance, is the passing on of traits from parents to their offspring; either through asexual reproduction or sexual reproduction, the offspring cells or organisms acquire the genetic information of their parents. Through heredity, variations between individuals can accumulate and cause species to evolve by natural selection. The study of heredity in biology is genetics.

YouTube Encyclopedic

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  • Heredity: Crash Course Biology #9
  • Introduction to Heredity
  • DNA, Chromosomes, Genes, and Traits: An Intro to Heredity
  • Heredity- Why you look the way you do?
  • Inheritance Explained || How do we inherit features from our parents?


So, I have this brother, John. You may have heard of him. JOHN: Hi there! HANK: As it happens, John and I have the exact same parents. JOHN: Yes, Mom and Dad Green. HANK: And since we have the same parents, it's to be expected that John and I would have similar physical characteristics because the source of our DNA is exactly the same. JOHN: Hank and I share some genes, but nobody knew anything about chromosomes or DNA until the middle of the 20th century. And people have been noticing that brothers tend to look alike since like, people started noticing stuff or whatever. HANK: That was very scientific, John. JOHN: I will remind you that I am doing you a favor. Heredity: it's basically just the passing on of genetic traits from parents to offspring. Like John said, the study of heredity is ancient, although the first ideas about how the goods are passed on from parents to kids were really really really really really really wrong. For instance, the concept that people were working with for nearly 2,000 years came from Aristotle, who suggested that: We're each a mixture of our parents' traits, with the father kind of supplying the life force to the new human and the mother supplying the building blocks to put it all together. Aristotle also thought that semen was like highly-purified menstrual blood, which is why we still refer to "bloodlines" when we're talking about heredity. Anyway, since nobody had a better idea, and since nobody really wanted to tangle with Aristotle, for hundreds of years everybody just assumed that our parents' traits just sort of blended together in us: like if a black squirrel and a white squirrel fell in love and decided to start a family together, their offspring would be gray. The first person to really start studying and thinking about heredity in a modern way was this Austrian monk named Gregor Mendel and Mendel demonstrated that inheritance followed particular patterns. In the mid-1800s, Mendel spent sort of an unhealthy amount of time grubbing around in his garden with a bunch of pea plants, and through a series of experiments, crossing the pea plants and seeing which traits got passed on and which didn't--he came up with a framework for understanding how traits actually get passed from one generation to another. So, to talk about Classical Genetics, which includes Mendel's ideas about how traits get passed along from parents to children, we kind of have to simplify the crap out of genetics. I hope you don't mind. So we've all got chromosomes, which are the form that our DNA takes in order to get passed on from parent to child. Human cells have 23 pairs of chromosomes. Now a gene is a section of DNA in a specific location on a chromosome that contains information that determines a trait. Of course, the vast majority of the time, a physical trait is a reflection of a bunch of different genes working together, which makes this all very confusing, and when this happens it's called a polygenic trait. Polygenic: many genes. And then again, sometimes a single gene can influence how multiple traits are going to be expressed; these genes are called pleiotropic. However, some very few, but some single traits are decided by a single gene. Like the color of pea flowers for example, which is what Mendel studied when he discovered all of this stuff, and when that happens, in Mendel's honor, we call it a Mendelian trait. There are a couple of examples of Mendelian traits in humans, one of them being the relative wetness or dryness of your ear wax. So, there is just one gene that determines the consistency of your earwax, and that gene is located at the very same spot on each person's chromosome. Right here! Chromosome 16. However, there's one version of this gene, or allele, that says the wax is going to be wet, and there's another allele that says the wax is going to be dry. You may be asking yourself what the difference is between these two things and I'm glad you asked because we actually know the answer to that question. Among the many amino acids that make up this particular gene sequence, there is one exact slot where they're different. If the amino acid is glycine in that slot, you're gonna have wet ear wax. But if it's arginine, it's dry. Now comes the question of how you get what you get from your parents. In most animals, basically any cell in the body that isn't a sperm or an egg -- these are called somatic cells -- are diploid, meaning there are two sets of chromosomes, one inherited from each of your parents. So you get one earwax-determining allele from your mom and one from your dad. I should mention that the reason for this is that gametes, or sex cells--Senor Sperm and Madame Egg--are haploid cells, meaning they only have one set of chromosomes. Again, for emphasis, non-sex cells are called somatic cells and they are diploid. Sex cells are gametes and they are haploid. This makes a lot of sense because a sperm or an egg has a very specific motivation: they're seriously hoping to score, and if they do, they plan to join with a complementary haploid cell that has the other pair of chromosomes they're going to need to make a new human, or buffalo or squid or whatever. Also, just so you know, some plants have polyploid cells, which means they have more than two sets of chromosomes in each cell, which isn't better or anything--it's just how they do. But anyway, the point of all that is that we inherit one version of the earwax gene from each of our parents. So, back to earwax! So, let's just say your mom gives you a wet earwax allele and your dad gives you a dry earwax allele. Good Lord, your dad has horribly ugly ears! Anyway, since your parents have two alleles, each for one gene inherited from each of their parents, the one passed along to you is entirely random. So, a lot of what Mendel discovered is that when there are two alleles that decide the outcome of a specific trait, one of these alleles could be dominant and the other one recessive. Dominance is the relationship between alleles in which one allele masks or totally suppresses the expression of another allele. So, back to earwax, because I know we all love talking about it so much. It turns out that Mom's wet earwax allele is dominant, which is why she gets a BIG W, and Dad's dry earwax allele is recessive, which is why he has to be a little w. JOHN: Go, Mom! HANK: Oh, you're back! JOHN: Yeah! You sound surprised. HANK: Anyway, Mom's allele is dominant, and that settles it, right-- we're gonna have wet earwax? JOHN: Uh, something about the way that you said that tells me it's not that easy. HANK: Aw, you are so much smarter than you look. It is indeed not that easy. So, just because an allele is recessive doesn't mean it's less common in all your genetic material than the dominant allele. Which leads us to the assumption, the CORRECT assumption, that there's something else going on here. JOHN: I'm definitely getting that vibe from you. HANK: So, it has to do with Mom and Dad's parents. Because everybody inherits two alleles from their parents. Mom got one from Nanny and one from Paw Paw. And let's just say Mom got a little w from Nanny and a big W allele from Paw Paw. That means Mom's genotype, or genetic makeup when it comes to that single trait, is heterozygous, which means she inherited two different versions of the same gene from each of her parents. Dad, on the other hand is a homozygote. JOHN: Let me guess, that means that he had two of the same allele, either a little w or a Big W allele inherited from both Grandma and Grandpa. HANK: Right! And in order for this to all work out the way that I want it to, let's just say that both Grandma and Grandpa would have passed little w's down to Dad, making his genotype homozygous recessive for this gene. JOHN: Okay, so I'm keeping score in my head right now. And according to my brain, Mom is a Big W, little w and Dad is a little w, little w. HANK: And now we're going to figure out what our earwax phenotype is. And phenotype is what's expressed physically, or in this case, what you'd see if you looked into our ears. JOHN: Alright, so are we gonna do a Punnett Square or anything? This is why I do history, if we're going to do Punnett Squares, I'm leaving! HANK: But I was just going to start to talk about people again. So Reginald C. Punnett, who was a total Gregor Mendel fanboy, invented the Punnett Square as a way to diagram the outcome of a particular cross breeding experiment. A really simple one looks like this: So, let's put Mom on the side here and give her a Big W and a little w. And let's put Dad on the top, and he gets two little w's. So if you fill this in, it looks like there's a 50/50 chance that any child of this mating will be homozygous or heterozygous. And as for our phenotype, it shakes out the same way: John and I both have a 50% chance of having wet ear wax and a 50% chance of having dry ear wax. So I just had to go and call John, because now he's not participating because he doesn't like Punnett Sauares, and it turns out, that he has wet ear wax. I also have wet ear wax. Which, you know, is not that unlikely, considering that our parents were homozygous and heterozygous. This may explain the odor of our bathroom growing up because it turns out there's a correlation between wet ear wax and body odor, because ear wax and armpit sweat are produced by the same type of gland. Because this one gene has an effect on multiple traits or phenotypes, it's an example of a pleiotropic gene, because the gene affects how wet your ear wax is, and how much you stink. One more thing you might find interesting: sex-linked inheritance. So we've got 23 chromosomes: 22 pairs are autosomes, or non-sex chromosomes, and 1 pair the 23rd pair, to be exact--is a sex chromosome. At that 23rd pair, women have two full length chromosomes, or "XX," and men have one X chromosome (that they inherited from their Mom) and this one little, short, puny, shriveled chromosome that we call "Y," which is why men are "XY." So, certain genetic traits are linked to a person's sex and are passed on through the sex chromosomes. Since dudes don't have two full chromosomes on pair 23, there may be recessive alleles on the X that they inherited from their mom that will get expressed, since there's not any information on the Y chromosome to provide the possibility for a dominant allele counteracting that specific trait. Take, for instance, balding. Women rarely go bald in their youth like some men do because it is caused by a recessive allele located in a gene on the X chromosome. So it's rare that women get 2 recessive alleles. But men need just one recessive allele and, Doh! Baldy bald! And that allele is on their X chromosome, which they got from Mom. But was Mom bald? Probably not. And where did Mom get that allele on her X chromosome? Either from her Dad or her Mom. So if you're bald, you can go ahead and blame it on your maternal grandmother, or your maternal-maternal great-grandfather or your maternal-maternal-maternal great-great grandfather who probably went bald before he was 30. So, Genetics, you guys. Resistance is futile. Thanks to my brother John for sharing his personal genetic information with us, and also his face and voice and all that stuff. That was very nice. Think of us next time you swab out your ears! Actually they say that you really shouldn't do that because we have earwax for a reason, and you might poke your brain or something. Okay, that's the last time I'm mentioning earwax. Review! Click on any of these things to go back to that section of the video. If you have any questions, please ask them in the comments.


Heredity of phenotypic traits: a father and son with prominent ears and crowns.
DNA structure. Bases are in the centre, surrounded by phosphate–sugar chains in a double helix.

In humans, eye color is an example of an inherited characteristic: an individual might inherit the "brown-eye trait" from one of the parents.[1] Inherited traits are controlled by genes and the complete set of genes within an organism's genome is called its genotype.[2]

The complete set of observable traits of the structure and behavior of an organism is called its phenotype. These traits arise from the interaction of the organism's genotype with the environment.[3] As a result, many aspects of an organism's phenotype are not inherited. For example, suntanned skin comes from the interaction between a person's genotype and sunlight;[4] thus, suntans are not passed on to people's children. However, some people tan more easily than others, due to differences in their genotype:[5] a striking example is people with the inherited trait of albinism, who do not tan at all and are very sensitive to sunburn.[6]

Heritable traits are known to be passed from one generation to the next via DNA, a molecule that encodes genetic information.[2] DNA is a long polymer that incorporates four types of bases, which are interchangeable. The Nucleic acid sequence (the sequence of bases along a particular DNA molecule) specifies the genetic information: this is comparable to a sequence of letters spelling out a passage of text.[7] Before a cell divides through mitosis, the DNA is copied, so that each of the resulting two cells will inherit the DNA sequence. A portion of a DNA molecule that specifies a single functional unit is called a gene; different genes have different sequences of bases. Within cells, the long strands of DNA form condensed structures called chromosomes. Organisms inherit genetic material from their parents in the form of homologous chromosomes, containing a unique combination of DNA sequences that code for genes. The specific location of a DNA sequence within a chromosome is known as a locus. If the DNA sequence at a particular locus varies between individuals, the different forms of this sequence are called alleles. DNA sequences can change through mutations, producing new alleles. If a mutation occurs within a gene, the new allele may affect the trait that the gene controls, altering the phenotype of the organism.[8]

However, while this simple correspondence between an allele and a trait works in some cases, most traits are more complex and are controlled by multiple interacting genes within and among organisms.[9][10] Developmental biologists suggest that complex interactions in genetic networks and communication among cells can lead to heritable variations that may underlie some of the mechanics in developmental plasticity and canalization.[11]

Recent findings have confirmed important examples of heritable changes that cannot be explained by direct agency of the DNA molecule. These phenomena are classed as epigenetic inheritance systems that are causally or independently evolving over genes. Research into modes and mechanisms of epigenetic inheritance is still in its scientific infancy, but this area of research has attracted much recent activity as it broadens the scope of heritability and evolutionary biology in general.[12] DNA methylation marking chromatin, self-sustaining metabolic loops, gene silencing by RNA interference, and the three dimensional conformation of proteins (such as prions) are areas where epigenetic inheritance systems have been discovered at the organismic level.[13][14] Heritability may also occur at even larger scales. For example, ecological inheritance through the process of niche construction is defined by the regular and repeated activities of organisms in their environment. This generates a legacy of effect that modifies and feeds back into the selection regime of subsequent generations. Descendants inherit genes plus environmental characteristics generated by the ecological actions of ancestors.[15] Other examples of heritability in evolution that are not under the direct control of genes include the inheritance of cultural traits, group heritability, and symbiogenesis.[16][17][18] These examples of heritability that operate above the gene are covered broadly under the title of multilevel or hierarchical selection, which has been a subject of intense debate in the history of evolutionary science.[17][19]

Relation to theory of evolution

When Charles Darwin proposed his theory of evolution in 1859, one of its major problems was the lack of an underlying mechanism for heredity.[20] Darwin believed in a mix of blending inheritance and the inheritance of acquired traits (pangenesis). Blending inheritance would lead to uniformity across populations in only a few generations and then would remove variation from a population on which natural selection could act.[21] This led to Darwin adopting some Lamarckian ideas in later editions of On the Origin of Species and his later biological works.[22] Darwin's primary approach to heredity was to outline how it appeared to work (noticing that traits that were not expressed explicitly in the parent at the time of reproduction could be inherited, that certain traits could be sex-linked, etc.) rather than suggesting mechanisms.[citation needed]

Darwin's initial model of heredity was adopted by, and then heavily modified by, his cousin Francis Galton, who laid the framework for the biometric school of heredity.[23] Galton found no evidence to support the aspects of Darwin's pangenesis model, which relied on acquired traits.[24]

The inheritance of acquired traits was shown to have little basis in the 1880s when August Weismann cut the tails off many generations of mice and found that their offspring continued to develop tails.[25]


Aristotle's model of inheritance. The heat/cold part is largely symmetrical, though influenced on the father's side by other factors, but the form part is not.

Scientists in Antiquity had a variety of ideas about heredity: Theophrastus proposed that male flowers caused female flowers to ripen;[26] Hippocrates speculated that "seeds" were produced by various body parts and transmitted to offspring at the time of conception;[27] and Aristotle thought that male and female fluids mixed at conception.[28] Aeschylus, in 458 BC, proposed the male as the parent, with the female as a "nurse for the young life sown within her".[29]

Ancient understandings of heredity transitioned to two debated doctrines in the 18th century. The Doctrine of Epigenesis and the Doctrine of Preformation were two distinct views of the understanding of heredity. The Doctrine of Epigenesis, originated by Aristotle, claimed that an embryo continually develops. The modifications of the parent's traits are passed off to an embryo during its lifetime. The foundation of this doctrine was based on the theory of inheritance of acquired traits. In direct opposition, the Doctrine of Preformation claimed that "like generates like" where the germ would evolve to yield offspring similar to the parents. The Preformationist view believed procreation was an act of revealing what had been created long before. However, this was disputed by the creation of the cell theory in the 19th century, where the fundamental unit of life is the cell, and not some preformed parts of an organism. Various hereditary mechanisms, including blending inheritance were also envisaged without being properly tested or quantified, and were later disputed. Nevertheless, people were able to develop domestic breeds of animals as well as crops through artificial selection. The inheritance of acquired traits also formed a part of early Lamarckian ideas on evolution.[citation needed]

During the 18th century, Dutch microscopist Antonie van Leeuwenhoek (1632–1723) discovered "animalcules" in the sperm of humans and other animals.[30] Some scientists speculated they saw a "little man" (homunculus) inside each sperm. These scientists formed a school of thought known as the "spermists". They contended the only contributions of the female to the next generation were the womb in which the homunculus grew, and prenatal influences of the womb.[31] An opposing school of thought, the ovists, believed that the future human was in the egg, and that sperm merely stimulated the growth of the egg. Ovists thought women carried eggs containing boy and girl children, and that the gender of the offspring was determined well before conception.[32]

An early research initiative emerged in 1878 when Alpheus Hyatt led an investigation to study the laws of heredity through compiling data on family phenotypes (nose size, ear shape, etc.) and expression of pathological conditions and abnormal characteristics, particularly with respect to the age of appearance. One of the projects aims was to tabulate data to better understand why certain traits are consistently expressed while others are highly irregular.[33]

Gregor Mendel: father of genetics

Table showing how the genes exchange according to segregation or independent assortment during meiosis and how this translates into Mendel's laws

The idea of particulate inheritance of genes can be attributed to the Moravian[34] monk Gregor Mendel who published his work on pea plants in 1865. However, his work was not widely known and was rediscovered in 1901. It was initially assumed that Mendelian inheritance only accounted for large (qualitative) differences, such as those seen by Mendel in his pea plants – and the idea of additive effect of (quantitative) genes was not realised until R.A. Fisher's (1918) paper, "The Correlation Between Relatives on the Supposition of Mendelian Inheritance" Mendel's overall contribution gave scientists a useful overview that traits were inheritable. His pea plant demonstration became the foundation of the study of Mendelian Traits. These traits can be traced on a single locus.[35]

Modern development of genetics and heredity

In the 1930s, work by Fisher and others resulted in a combination of Mendelian and biometric schools into the modern evolutionary synthesis. The modern synthesis bridged the gap between experimental geneticists and naturalists; and between both and palaeontologists, stating that:[36][37]

  1. All evolutionary phenomena can be explained in a way consistent with known genetic mechanisms and the observational evidence of naturalists.
  2. Evolution is gradual: small genetic changes, recombination ordered by natural selection. Discontinuities amongst species (or other taxa) are explained as originating gradually through geographical separation and extinction (not saltation).
  3. Selection is overwhelmingly the main mechanism of change; even slight advantages are important when continued. The object of selection is the phenotype in its surrounding environment. The role of genetic drift is equivocal; though strongly supported initially by Dobzhansky, it was downgraded later as results from ecological genetics were obtained.
  4. The primacy of population thinking: the genetic diversity carried in natural populations is a key factor in evolution. The strength of natural selection in the wild was greater than expected; the effect of ecological factors such as niche occupation and the significance of barriers to gene flow are all important.

The idea that speciation occurs after populations are reproductively isolated has been much debated.[38] In plants, polyploidy must be included in any view of speciation. Formulations such as 'evolution consists primarily of changes in the frequencies of alleles between one generation and another' were proposed rather later. The traditional view is that developmental biology ('evo-devo') played little part in the synthesis, but an account of Gavin de Beer's work by Stephen Jay Gould suggests he may be an exception.[39]

Almost all aspects of the synthesis have been challenged at times, with varying degrees of success. There is no doubt, however, that the synthesis was a great landmark in evolutionary biology.[40] It cleared up many confusions, and was directly responsible for stimulating a great deal of research in the post-World War II era.

Trofim Lysenko however caused a backlash of what is now called Lysenkoism in the Soviet Union when he emphasised Lamarckian ideas on the inheritance of acquired traits. This movement affected agricultural research and led to food shortages in the 1960s and seriously affected the USSR.[41]

There is growing evidence that there is transgenerational inheritance of epigenetic changes in humans[42] and other animals.[43]

Common genetic disorders


An example pedigree chart of an autosomal dominant disorder.
An example pedigree chart of an autosomal recessive disorder.
An example pedigree chart of a sex-linked disorder (the gene is on the X chromosome).

The description of a mode of biological inheritance consists of three main categories:

1. Number of involved loci
2. Involved chromosomes
3. Correlation genotypephenotype

These three categories are part of every exact description of a mode of inheritance in the above order. In addition, more specifications may be added as follows:

4. Coincidental and environmental interactions
5. Sex-linked interactions
6. Locus–locus interactions

Determination and description of a mode of inheritance is also achieved primarily through statistical analysis of pedigree data. In case the involved loci are known, methods of molecular genetics can also be employed.

Dominant and recessive alleles

An allele is said to be dominant if it is always expressed in the appearance of an organism (phenotype) provided that at least one copy of it is present. For example, in peas the allele for green pods, G, is dominant to that for yellow pods, g. Thus pea plants with the pair of alleles either GG (homozygote) or Gg (heterozygote) will have green pods. The allele for yellow pods is recessive. The effects of this allele are only seen when it is present in both chromosomes, gg (homozygote). This derives from Zygosity, the degree to which both copies of a chromosome or gene have the same genetic sequence, in other words, the degree of similarity of the alleles in an organism.

See also


  1. ^ Sturm RA; Frudakis TN (2004). "Eye colour: portals into pigmentation genes and ancestry". Trends Genet. 20 (8): 327–332. doi:10.1016/j.tig.2004.06.010. PMID 15262401.
  2. ^ a b Pearson H (2006). "Genetics: what is a gene?". Nature. 441 (7092): 398–401. Bibcode:2006Natur.441..398P. doi:10.1038/441398a. PMID 16724031. S2CID 4420674.
  3. ^ Visscher PM; Hill WG; Wray NR (2008). "Heritability in the genomics era – concepts and misconceptions". Nat. Rev. Genet. 9 (4): 255–266. doi:10.1038/nrg2322. PMID 18319743. S2CID 690431.
  4. ^ Shoag J; et al. (Jan 2013). "PGC-1 coactivators regulate MITF and the tanning response". Mol Cell. 49 (1): 145–157. doi:10.1016/j.molcel.2012.10.027. PMC 3753666. PMID 23201126.
  5. ^ Pho LN; Leachman SA (Feb 2010). "Genetics of pigmentation and melanoma predisposition". G Ital Dermatol Venereol. 145 (1): 37–45. PMID 20197744. Archived from the original on 2019-03-28. Retrieved 2013-03-26.
  6. ^ Oetting WS; Brilliant MH; King RA (1996). "The clinical spectrum of albinism in humans and by action". Molecular Medicine Today. 2 (8): 330–335. doi:10.1016/1357-4310(96)81798-9. PMID 8796918.
  7. ^ Griffiths, Anthony, J.F.; Wessler, Susan R.; Carroll, Sean B.; Doebley J (2012). Introduction to Genetic Analysis (10th ed.). New York: W.H. Freeman and Company. p. 3. ISBN 978-1-4292-2943-2.{{cite book}}: CS1 maint: multiple names: authors list (link)
  8. ^ Futuyma, Douglas J. (2005). Evolution. Sunderland, Massachusetts: Sinauer Associates, Inc. ISBN 978-0-87893-187-3.
  9. ^ Phillips PC (2008). "Epistasis – the essential role of gene interactions in the structure and evolution of genetic systems". Nat. Rev. Genet. 9 (11): 855–867. doi:10.1038/nrg2452. PMC 2689140. PMID 18852697.
  10. ^ Wu R; Lin M (2006). "Functional mapping – how to map and study the genetic architecture of dynamic complex traits". Nat. Rev. Genet. 7 (3): 229–237. doi:10.1038/nrg1804. PMID 16485021. S2CID 24301815.
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  13. ^ Bossdorf, O.; Arcuri, D.; Richards, C.L.; Pigliucci, M. (2010). "Experimental alteration of DNA methylation affects the phenotypic plasticity of ecologically relevant traits in Arabidopsis thaliana" (PDF). Evolutionary Ecology. 24 (3): 541–553. doi:10.1007/s10682-010-9372-7. S2CID 15763479. Archived (PDF) from the original on 2020-03-01. Retrieved 2019-08-15.
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