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Crossing over primarily happens because of homologous recombination (HR). From the molecular point of view, it can happen between any homologous regions and it is not necessary that an entire allele has to be crossed over. During the process of HR, a DNA double strand break occurs. This is followed by resection (exonucleolytic degradation from 5'→3') by the ...


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These regions, if unannotated, are simply called intergenic regions. Sometimes, if a large section of chromatin is regulated by an enhancer/silencer/locus control element, then there are boundary elements that demarcate this chromatin region and prevent the spread of the chromatin state to neighbouring regions.


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The straight forward answer is: we don't know. We don't have any direct evidence for what happened at that time nor any completely developed and coherent theories for how it worked. The widely believed hypothesis is the "RNA World" hypothesis. RNA, unlike DNA, is capable of spontaneously folding to form catalytic molecules and thus avoids the needs for ...


0

As you correctly discerned, distinguishing the fetal cell free DNA from the mothers cell free DNA in the blood stream is one of the major challenges in this type of diagnostics. Consequently, the results that can be directly linked to the paternal DNA are the most reliable. In the case of the example you give, the high accuracy stems from the fact that in ...


2

As Matej said, mutations in two different genes (or even a gene and a non-coding regulatory element) can lead to complementation and as they pointed out, the complementation test is designed to check if mutations are on separate genes or not. Molecular mechanisms that may lead to complementation (apart from Matej's example): The double mutation in two ...


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The main principle is that the loss-of-function mutations have to be on different genes and recessive. Source I wouldn't say they compensate each other. If either of them was in homozygous conformation, their effect would be full-shown. The thing on the molecular level is that often less than 50 % of the gene product is necessary for the gene to "work", to ...


0

I was wondering if there is a mechanism that can give priority to certain genes to be accurately duplicated. Some sort of trigger that says "double-check this specific gene before continuing with the duplication". A mechanism that would say: "double check this part, it's important" isn't known to me neither, but if I understood your question ...


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I suppose unligated oligonucleotide would also be "amplified" but on much lesser scale(?only one part of probe?). For instance after 6th run of PCR you would get 2^6=64 amplicons of ligated probe but only 6 for one unligated part(?second starter is designed to anneal to second part of antisense oligonucletide of probe?). After 30 runs there is massive ...


3

Both genes and alleles are sequences of DNA. A gene will code for a trait, say hair colour, while an allele will be the variants of that gene (say the alleles coding for blonde, brown, black, and red hair). It's almost like cookbooks: two cookbooks (the DNA) might have a recipe (gene) for bread but they use slightly different instructions (alleles) ...


5

Alleles are basically subtypes of a gene. At the time of Mendel, the molecular nature of inheritance was not known so the original definition of gene refers to "some" inheritable molecular entity inside the organism that is responsible for a trait. Alleles are different "flavours" of a given gene. For example there is a gene for flower colour, there can be ...


1

ChIP-seq isn't perfect. Even between technical replicates, you get a fair amount of variation, especially for broad marks like those you're using. It's rather uncommon to see people use H3K79me2 and H3K36me3 to determine if a gene's expressed or not. Using H3K4me3 and H3K27ac or H3ac is a more common method of marking promoters of transcribed genes. 40 ...


3

It is difficult to draw any conclusion without further experimentation. There may be many other factors that prevent the expression of the gene including factors like post-transcriptional regulators. Some histone modifications like the ones you are mentioning are also a bit dicey and there can be bivalent modifications too. However, if there is a strong ...


2

There is a large amount of variation in the distribution and number of chiasmata or crossing overs (COs). The total number of chiasmata per cell can vary within the same organism. Where chiasmata occur along the chromosome is also not consistent cell to cell. Hotspots are 1-2kb regions that experience elevated recombination compared to neighboring genomic ...


4

Is the gene coding for the transcriptional factor always present next to (or close to) the transcription unit? Not necessarily. You can find several counter-examples. Even for prokaryotes this is not necessarily true. The genes regulated by a common factor are called regulons and though the target genes need not be proximal to the regulator, it has ...


0

In replication you have 2 strands made. In transcription you have 1 strand made. Transcription uses ONLY the 3' → 5' DNA strand. This eliminates the need for the Okazaki fragments seen in DNA replication (on the lagging strand). And it removes the need for a RNA primer to initiate RNA synthesis, as is the case in DNA replication. Edit; instead RNA ...



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