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16

Lethal genes evolve simply because of random deleterious mutations and absence of strong selection. Recessive lethal genes Random mutations can make a gene product non-functional or reduce its activity. However, in diploid organisms the other fully-functional copy of the gene can compensate for the non-functional allele. Sometimes both the alleles can ...


11

Your individual questions here are reasonable enough - although you could do a bit better at knowing some more details of the systems you are dismissing as 'flawed'. However, I think the bigger problem is your overall approach, which seems to be to make analogies between human-made computers and biological systems and then critiquing the 'missing' parts from ...


7

In programming, if you need to ensure your data has integrity, a single array won't do. We have cyclic dependency checks in programing to determine if the data is corrupt. We have hamming codes to permit detecting a fixing one bit corruption. If we want to really fix multi-bit corruption, we need at least one copy of the data. Lossless compression ...


7

(For the direct answer to your question skip to the end!) Genetic linkage can affect the spread of other genes. The degree of linkage, affected by the rate of recombination between the point (nucleotide, gene etc.) directly under selection and the other point. If the rate of recombination between to given points is low then linkage between them is high and ...


5

Genetic hitchhiking / genetic draft From wikipedia Genetic hitchhiking, also called genetic draft or the hitchhiking effect, is when an allele changes frequency not because it itself is under natural selection, but because it is near another gene on the same chromosome that is undergoing a selective sweep. The term "selective sweep" is used improperly ...


5

So the term allele is a broad one, and simply refers to the different versions of any piece of DNA in circulation in the gene pool - it doesn't need to refer to a gene. I can talk about the alleles at a random place in the genome. But if we proceed with your question and ask - 'do nonsense mutations within coding genes also lead to the creation of different ...


4

This is just loose terminology. By ‘lethal gene’ Dawkins means an essential gene with a mutation that renders it inactive. With a recessive gene, the one ‘good’ copy in the heterozygote provides enough gene-product to allow survival, in contrast to the situation in the homozygote where the total absence of gene-product is lethal. With a rare mutation, the ...


3

Is there evidence of selection against long proteins and long genes? I am not aware of any such evidence and cursory googling did not reveal studies that researched a correlation between gene selection and gene size. However, the larger a gene, the larger the probability of a deleterious mutation within said gene so I expect that there is some limit to ...


3

Mutations are not performed targeting a specific new phenotype. There is no way an organism can "know" the impact of a specific future mutation anyway. A mutation is just a mistake in the replication process. As a consequence the majority of mutations are deleterious and only a handful of mutations are beneficial. It is true though that the mutation rate ...


3

Assuming... The parents are the real biological parents (no cheating allowed!) There is a purely dominance/recessivity relationship between the alleles and no individual can express the disorder without being homozygous for the disease causes allele De novo mutations for the disorder are rare enough to be ignored in the calculation of this probability ...


3

I would say that first exception might be White gene in Drosophila Melanogaster, described in 1910 by Thomas Hunt Morgan and Lilian Vaughan Morgan. At least, is the first exception we study in genetics since sex linkage its so fundamental. These experiments established the chromosomal theory of inheritance. Thomas Hunt Morgan, an embryologist who had ...


3

To add to Remi b's answer - this question is confusing because 'null' and 'recessive' are terms emerging from two very different levels of analysis. The concept of 'recessive' existed before we knew what genes were, or how they worked. It just describes the patterns of inheritance you see in a gene's effects. The concept of a 'null' allele however came ...


2

Allele is just a variant form of gene: independent of the final product of protein, so nonsense will also lead to new allele. I will quote Nature Scitable here: Alleles can also refer to minor DNA sequence variations between alleles that do not necessarily influence the gene's phenotype.


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The term sister chromatids refers to the pair of chromosomes which have been produced from a single parent chromatid by DNA replication, while a homologous pair refers to chromosomes which are more distantly related (e.g. those inherited from one's mother and father, which I guess is what you mean by 'male and female chromosome'). So the two options you ...


2

After a lot of research, I've finally found an answer. In the case of humans, it is practically impossible. See this article from wikipedia: During gestation, the cells of the primordial gonad that lie along the urogenital ridge are in a bipotential state, meaning they possess the ability to become either male cells (Sertoli and Leydig cells) or female ...


2

Good question +1. Unfortunately, the mechanisms by which dominance work is relatively poorly understood and it is likely that the mechanism differs from one locus to another. You might want to have a look at the posts Why are some genes dominant over others? What is the mechanism behind it? Evolution of dominance or some papers such as Llaurens et al. ...


2

The coefficient of relationship between you and your uncle is 25% (see wiki > coefficient of relationship for more info). However, the percentage of similarity depends on the genetic diversity in the population of interest. If you were studying a population of fully homozygous clones (no genetic diversity), then no matter what the coefficient of ...


2

The first exception to Mendelian genetics was probably discovered by Mendel. As a followup to his pea experiments, Mendel used hawkweed, in which his rules do not seem to apply due to some unusual aspects of hawkweed development; see Apomixis in hawkweed: Mendel's experimental nemesis for details. Mendel eventually abandoned his biological experiments, ...


2

[H]ow exactly we mark out genotype in science? Do we use D's and r's? General rule The general rule is to indicate the dominant allele with a upper-case letter and the recessive allele with a lower-case letter. The most commonly used letter is the first letter of the alphabet. The two possible alleles are a and A and the four possible genotypes here ...


2

This kind of question is what developmental genetics is all about. The answer turns out to be, in general, 'no'. There is no neat mapping between spatial dimensions of an organism and its genome. (There is one exception to this in some organisms called the Hox cluster, but they are kind of a freak case). The reason for this is that in general you should ...


2

In population genetics, with a simple one-locus two-allele model, we consider the frequency of the two alleles to be $p$ and $q$ where $p + q = 1$ (and thus $1-p=q$ and $1-q=p$). When an allele is recessive it is only expressed at the phenotypic level when the individual carries two copies of the allele. Following from your example, gene $A$ might be ...


1

This is an open-ended question and will be impossible to correctly answer. I am voting "to close as too broad". Note also that the question in the title is not the same as the question in the post. But I still wanted to give you some information that may help you. Here are just a few examples for which knowing gene density matters. Background selection ...


1

Largely an informed guess based on properties of distributions rather than specific knowledge of statistical genetics: a beta distribution is useful for modeling the frequencies of two alleles at one locus. A Dirichelet distribution, which is a multivariate generalization of a beta distribution, would thus be useful for modeling a set of loci. The flip side ...


1

Usually relatedness is described via the coefficient of relationship because it is natural, relatively simple to calculate, and corresponds well to the actual amount of DNA likely to be inherited. In this system, you are 50% related to your mother, and your mother is 50% related to her full brother (your uncle), so you are 50% $\times$ 50% $=$ 25% related ...


1

Issues with the post Sexual selection is a mode of natural selection where members of one biological sex choose mates of the other sex to mate with (intersexual selection), and compete with members of the same sex for access to members of the opposite sex (intrasexual selection). This question has nothing to do with sexual selection. What do you mean by ...


1

To some extent, it depends on what you mean by "dominance". If you take a phenotypic definition of dominance, then the answer is (technically) yes, you could imagine such a gene system. That is, imagining alleles p, q, and r, and three phenotypes P, Q, and R, with the following homozygous behavior: pp ➞ P qq ➞ Q rr ➞ R Then you could theoretically ...


1

Dominance by silencing the other allele The mechanisms by which dominance work are still very much unknown. One type of mechanism that will be of particular interest to this question is the modifier of dominance where the protein product of an allele silence the expression of the other allele in order to cause dominance relationship. Is the pattern you ...


1

Metrics of interest The two metrics you are interested in are $\pi$ - the mean number of differences between two randomly sampled (with replacement) alleles in a population $d$ - the mean number of differences between two randomly sampled (with replacement) alleles coming from two different species Consider two sequences ATCGTCAAT ATAGTTAAT There ...


1

I am assuming you are referring to the use of the software GTCA (which stands for Genome-Wide Complex Trait Analysis). Original paper: Yang et al. (2011). I looked to the papers who cited Yang et al. (2011) and quickly scanned through looking for "leg". I did not find anything on it. So my best guess is: No, nobody ever applied GTCA to leg length.


1

Yes, having a Y chromosome does cause specific alterations to facial structure. The Y chromosome doesn't contain much actual genetic information. Most of the information needed to activate the male developmental program (the female one is the default) is in just one gene 'SRT', the other genes on the Y chromosome aren't super important, such that you can ...



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