New answers tagged genetics
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This is one of the reasons the 1000 genomes project was created.
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You might be able to get some raw data on SNP frequency by batch querying the dbSNP database. I have not used it myself, though.
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You can use power analysis to work out answers depending on the specifics of your data. The things you need to consider are:
The power of the test. This is the probability that the test will
fail to reject the null hypothesis even if in truth it is false
(Type II error). If the population is not in equilibrium, what is
the probability that the test will ...
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In order:
Unfortunately, there's no easy way to batch query with only location. You could look up SNPs within genes here. (You could find the gene a SNP is located in by searching an annotated human genome file for the position.)
You can figure out whether it's in 3'UTR by comparing to a list of human 3' UTRs. The UCSC genome browser page here will help: ...
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The sequence is believed to be opposite of that implied by the phrasing of the question: the inheritance of structures supporting inheritance came before protocells. The important point is that you need a system of reproduction before building more complicated structures (such as a cell). Without replication (reproduction), a cell would be little more than ...
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The general theory is RNA came first, then DNA. Both are able to replicate with simple changes in temperature (see polymerase chain reaction). So if we imagine a world with nucleotides making RNA, the idea is the survival of the fittest RNA. RNA for example that also had enzymatic activity was "fitter" than RNA that did not. Then go further down the line ...
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Here is a good overview of primer design considerations when using Gibson assembly.
http://j5.jbei.org/j5manual/pages/22.html
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This is controversial, but most groups in the field have concluded that RNAi does not work in the nucleus despite the presence of Ago. When lncRNA have been KD'd with RNAi, they are usually shown to be present in both the nucleus and cytoplasm, and the KD is thought to occur in the cytoplasm, not nucleus. Of course as always in biology it is possible that ...
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You can take a look at this tutorial to understand TCGA MAF files. And you can find a list of TCGA MAF files containing mutations mapped to genes and miRNA at https://www.synapse.org/#!Search:syn1710680
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Disclaimer: I haven't ever done a Gibson assembly, but here is my theoretical understanding of how to design your primers. You need four 40mers each consisting of 20 bp segments derived from the vector and the insert and corresponding to the junctions that you are trying to create. In the diagram below the dotted lines represent the junctions between the two ...
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Knockdown of lncRNA in mammals is not done via RNAi. Instead, one transfers antisense DNA oligos which bind to the RNA. This triggers the action of the RNase H enzyme, which degrades RNA-DNA duplexes. It degrades the lncRNA.
UPDATE: For reference, I learned about this from a seminar, and it is not very well documented, but after some literature search I ...
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Nuclear RNAi happens.. check these articles:
http://www.nature.com/nrg/journal/v14/n2/execsumm/nrg3355.html
http://nar.oxfordjournals.org/content/early/2011/11/07/nar.gkr891.full
Also there is some evidence that Ago2 binds to lncRNAs.
However, you can employ other techniques to knock down lncRNAs for e.g. ribozymes.
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This stage is after the adsorption of the adapter-ligated fragments on the flow cells.
The fragments are isothermally amplified to generate clusters [1]. The exact nature of the enzyme mix that catalyses this step is not disclosed by Illumina. I assume it must be similar to Helicase mediated isothermal amplification, which uses helicase and single ...
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The v short answer is that in shotgun sequencing, the sequencer is fed a set of random sequences from the target. This can be done for instance by mechanically shearing DNA and then building a set of shotgun sequencing jobs which are then compiled back together by a genome assembler (i.e. in whole genome sequencing projects) into a full sequence.
In ...
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I think you may have been misled by graphic representations of the process: The actual replication fork is very small as, like Rex Kerr mentions, it costs a lot of energy to keep DNA single stranded.
Have a watch of https://www.youtube.com/watch?v=yqESR7E4b_8 at minute 1:45, it contains a relatively realistic representation of the replication fork. Of ...
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It's in fragments for efficiency. Single-stranded DNA is not very stable without proteins to stabilize it. If you tried to replicate the entire strand in one go, you'd need to keep the entire strand in single-stranded form one way or another (e.g. start at both ends and meet in the middle would still leave each half as an old/new duplex, plus an old ...
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In addition to @mgkrebbs response, I'd add that many genes are controlled by epigenetic mechanisms which may mask one of the parental copies by methylation. This can be a specific effect where, the active gene is specifically from either the father or the mother. Mosaicism, where one copy of gene is randomly inactivated in any given cell, is also possible. ...
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First, while half the chromosomes come from each of the two parents, these two sets of chromosomes are not termed X and Y (they would usually be called maternal and paternal). The terms X and Y refer to potential members of just one pair of the 23 pairs (in humans) of chromosomes, and X chromosomes can come from either the mother or the father. The ...
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What does it mean if gene A is epistatic to gene B? Does this simply mean that gene A masks the phenotype of gene B when expressed?
Yes. Note that this does not say anything about mechanism. If A converts 1 to 2, and B converts 2 to 3, then A is epistatic to B, but A is also upstream of B. In a signaling pathway, say B inhibits A and prevents it from ...
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In theory, your idea seems reasonable, but I can see at least to problems with implementing it.
First, the situation is complicated by the fact that genes often carry out multiple functions, and a single label is often insufficient to annotate the complete functional repertoire of a gene. @MichaelKuhn made an excellent point with regards to the evolution of ...
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I think it seems like a good idea at first but...
You have to take into account that as has been said genes might have multiple roles, sometimes very different and for most of them functions are still unknown.
So It's very difficult to classify a constatly changing promiscuous set of things. Even the gene concept is changing (Hello, ENCODE :)).
To me It's a ...
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Many gene names are descriptive, e.g. DRD1: dopamine receptor D1, TOP2A: DNA topoisomerase 2-alpha, or PTGS1: prostaglandin G/H synthase 1. These are examples of genes that have a clearly defined main function.
The genes you listed are involved in development, and there describing the function of a gene becomes much more difficult. E.g. sonic hedgehog is ...
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Are there are any efforts underway to systematize or name genes for a given organism in an expressive manner?
As you observed, the genes are named by their discoverers and some genes usually have anecdotes behind their names. Since gene names have to be small it is difficult to systematically describe them completely. But gene nomenclature can adopt a ...
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Quick answer: we don't really know.
As WYSIWYG said, splice sites do have a sequence signature. The image below (taken from [1]) shows the consensus for human acceptor and donor sites:
In the images above, the size of a nucleotide represents its frequency at that location. As you can see, there is a clear signal around the splice sites and this signal is ...
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There are some signature sequence which mark intron-exon boundaries. Usually introns start with a GU and end with an AG. But this feature per-se is not sufficient for splicing; there are other cis-elements such as exon/intron splicing enhancers/silencers [ESE/ESS; ISE/ISS]. Refer this article.
Also, there are protein regulators of splicing such as SR ...
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I'm Australian-born, with ancestry of about 7 European countries, and I've lived in Europe. Oregon and Virginia in my life. My (guessed/non-scientifically tested) theory is that Australians have adapted quite a bit to climate and surroundings, so have facial features as such. For example, rough(er) skin due to higher average temperatures and more sunburn ...
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Low complexity regions have repeats in nucleotides ( or amino acids ). E.g. PPCDPPPPPKDKKKKDDGPP or AAATAAAAAAAATAAAAAAT. This 2011 article compares 14 individual Plasmodium falciparum genomes and finds that these repeats are highly variable between individuals - some may be short AAAATAAAA others may be longer AAAATAAAAAAAAATAAAAAAATAAAATAAAA....AATAA ...
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Supplementary information from the Comments from the first answer:
I have perhaps found @terdon's reference? Not sure if this is it, but by measuring transcription events in individual cells, Taniguchi et al. certainly make the case that there is no correlation between protein and mRNA levels.
However microarray data (and most rnaSeq and qPCR ...
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The technique described here is called microarray. Your question has given me an opportunity to put forth one of my opinions about certain problems of gene expression studies.
Gene expression is a measure of the activity of any gene. If the gene performs its activity in the form of a protein, then its expression should be a measure of the protein. If a gene ...
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Wikipedia gives a very good explanation of this, on the page for the suprachiasmatic nucleus.
For example, in the fruitfly Drosophila, the cellular circadian rhythm
in neurons is controlled by two interlocked feedback loops.
In the first loop, the bHLH transcription factors clock (CLK) and
cycle (CYC) drive the transcription of their own ...
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Goods question! Only mutations that occurred when we were in the early stages of development will affect all cells. That's why pregnant mothers shouldn't smoke. The reason for this is that one cell goes on to divide and become all our cells so any mutations in that cell are passed on to cells formed when it divides. That same principle explains your smoker ...
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Are you sure it is 0.59 because I am getting 0.5625 for part (a) and this is how I computed.
To check genetic similarity of siblings we first have to pick up mating pairs. Six mating pairs possible with following offspring probabilities (choice of first mate x choice of second mate x same offspring genotype freq).
AA x AA : will always give same type of ...
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