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8

A pre-tRNA is transcribed from tRNA genes in DNA by RNA polymerase III. Processing occurs in the nucleus, where a 5' sequence is cleaved by RNase P, the 3's CCA motif is added, and ~10% of the nucleotides are substituted. The tRNA are transported out via the pore complexes. Aminoacyl-tRNA synthetase enzymes attach amino acids in the cytoplasm in a 2-step ...


7

When you travel to different time zones, your circadian clock will be off. The reason your circadian clock will be off is because your body has adapted to the time zone you are from. When you enter a new time zone, your circadian clock will still be functioning on the old the time zone. If the time zone difference is $\pm 12$ hours, this is a huge ...


7

Short answer: Pointers already exist within the genome, in terms of transcription elements (such as repressor/activator systems). These systems can remotely activate a specific gene for transcription based on concentrations of specific chemicals within the cell. The problem with LINEs are that they are thought to be ancient retroviruses which lost their ...


7

Parent 1 and 2 have each 5 possible genotypes (OO, AO, BB, BO and AB). Here a Punnett square with each possibilities. I highlighted the possible parent genotypes. The total number of possible crosses is exactly 21. Note that here A = Ia, B = Ib and O = i. OOxBB,OOxBO,OOxAB AOxBB,AOxBO,AOxAB BBxOO,BBxAO,BBxBB,BBxBO,BBxAB BOxOO,BOxBB,BOxAO,BOxBO,BOxAB ...


5

Multiple RNA Polymerase transcription complexes engaged on the lacZ gene at the same time, staggered along the gene.


5

A paper was published about a week ago in Nature Biotechnology and adresses your question, Maruyama T et al., 2015. I must say I found the authors' strategy extremely clever. It is not about increasing efficiency by reducing specificity, but simply increasing efficiency (which is your ultimate goal anyway). What the authors did was to inhibit nonhomologous ...


5

Ns are not non-recombinant at the genomic level. What you know is that they do not show recombination events at the risk allele locus as subjects carrying the marker A1 show signs of the disease and similarly healthy subject do not carry the marker A1. Hence they are called non-recombinant. On top of that 3rd generation subjects (excepted III6) show ...


4

Positive feedbacks can be one alternative. Positive feedbacks exhibit bistability and can therefore adopt one of the two stable states depending on the initial condition. A famous example of a positive feedback switch would be that between cI and Cro in λ-phage, which repress each other. Positive feedbacks also display hysteresis: if the state of the system ...


4

Claudia's dad is not a taster, so he is tt. He passes one allele on to his daughter. Since he is homozygous, he can only pass t. Claudia is a taster, so she must have the dominant allele from her mother, who is also a taster. Thus, Claudia is Tt.


4

Either the gene is present in multiple copies (especially possible if it is in a plasmid) or multiple RNA polymerases are transcribing it, each beginning from the start site one after the other with some amount of time delay, much like multiple ribosomes translate the same mRNA to increase rate of protein production.


3

The growth of blood vessels is called angiogenesis. This process occures during embrional development, tissue repair, and even tumor formation (in fact this is a crucial step for tumors to survive). This Nature review provides great overview of the process, I'll try and briefly summarize things: In general large arteries grow circumferential to keep up ...


3

SNPs are much denser than RFLPs and VNTRs therefore the DNA resolution is much greater with SNPs. VNTRs were historically used for linkage mapping while SNPs allowed for association studies (e.g. GWA studies). Therefore your question goes down to what are the differences between linkage mapping and association studies. They are both forward genetic methods ...


3

It is possible but extremely unlikely. When a base undergoes tautomeric shift the DNA does not contain a mutation yet, just an unmatched pair. The mutation will only becomes inscribed into the DNA permanently after the DNA is replicated or wrongly repaired. In order to reverse the mutation you would need to provoke a chemical change to that specific base ...


3

T-cell migration to the brain is very limited and occurs at a very low level in healthy conditions, however during diseases the number of T cells passing through the blood-brain barrier is elevate due to increased expression of traffic signals and adhesive molecules. I've found two good articles on how T-cells migrate through blood-brain barrier: J Neural ...


3

Conjugation occurs between cells of the same species too. For this to occur cell have to be close to each other. Now, if you have an isolated population of bacteria that never gets in contact with an F+ bacteria then this population would stay F-. Also not all conjugation events are successful, mechanical perturbations can disrupt the pilus through which ...


2

There are definitely genomic DNA sequences that nucleosomes preferentially package in vitro. They are A/T rich and have a periodic structure that facilitates bending. However such sequences would typically not be found on exons in vivo (because their protein-coding potential is reduced). Based on the accumulating literature, active promoters (and regions ...


2

Transcription interference can also be a good mechanism to provide such switches. Transcription interference occurs between genes in close adjacency to each other. This is basically, as the term suggest, that the neighbouring genes can interfere with each others transcription (by overlapping promoters blocking transcription initiation, collision of ...


2

First of all I am not sure if your examples are per se correct. But they might also be an additional bonus. Secondly, I would like to refer to two articles: "Polyploidy" and "The advantages and disadvantages of being polyploid". One of the main benefits could be allowing organisms long-term evolutionary flexibility. Often adapted polyploids can undergo a ...


2

Lets assume for simplicity that DNA is globally subjected to the same mutation rate (which is probably not a fully correct assumption). Now let take a DNA region which is functional (what you meant by giving a fitness benefit), mutations in this region will occur as anywhere else in the genome. Some mutations will be deleterious and reduce the fitness of ...


2

Question 1: The phenomena you describe in which it matters whether you have one or two copies of an allele (e.g., the AA phenotype being different than the Aa phenotype) are known as dominance effects. Dominance effects can interact with epistatic effects (in which the phenotypic effect of one locus depends on the genotype at the another locus). One good ...


2

From the pheno-geno map and the genotypes frequencies, you have the whole distribution of phenotypes in your population. The mean of the phenoype $n$, $P_n$ is the $$\bar P_n = \sum f_{G_i} P_{G_i}$$ , where $f_{G_i}$ is the proportions of individuals having genotype $G_i$ and $P_{G_i}$ is the phenotype of the individuals with genotype $G_i$. Therefore, ...


2

If you have genomic imprinting then $k^n=m^2$ (with k=m and n=2 because of diploidy) is correct as inheriting a from the father and b from the mother (i.e. ab) is not equivalent to inheriting b from the father and a from the mother (i.e. ba). For 3 alleles (a,b,c) you have 9 possible genotypes (aa,ab,ac,ba,bb,bc,ca,cb,cc). Under no genomic imprinting, ab ...


2

So in a pedigree, Standardized Human Pedigree Nomenclature: Update and Assessment of the Recommendations of the National Society of Genetic Counselors notes that these "nodes" in the pedigree are the "individual symbol" denoting individuals. Although, when you read it, you'd read "Male," "Female," "Gender Unspecified," etc. instead of individual symbol.


1

I assume these are all carcinogenic mutations. Because some them are clearly recessive loss-of-function mutations (like loss of transcript), you can conclude that the function of the gene consists of "holding back cancer". When these mutations occur, they can generally be complemented by a healthy allele on the sister chromosome. Oncogenes on the other ...


1

A: wild-type allele / a: color blind allele Because color blindness is recessive and X-linked your assumption $p=F(a)=4\%$ is correct as men do only have one copy of the allele. Subsequently $F(A)=q=1-p=0.96$ is also correct. Therefore: a) $F(Aa)=2pq=7.68\%$ is correct and b) is wrong, a is the color blind allele and $F(a)=0.04$ therefore it's ...


1

If you're looking at evolutionary timescales, then the only available source of information is the target organism's genome sequence. At least some of the methods of horizontal gene transfer you mention leave a distinctive signature in the genome. For example, retrovirus particles that have become incorporated into the human genome are easily identified by ...


1

Centi-Morgan (cM) is based on observation not precise measurements. Now since double crossing-overs (and actually any arbitrary even number of crossing-overs) revert gene combination to the parental type, resulting lower recombinant frequency. So in your case since the chance (or the frequency if you wish) for double COs is 0.6%, you have to subtract this ...


1

There are several subconcepts within the concept of robustness. Several definitions exist for all of these concepts and I am just suggesting one variant of the possible definitions below. Mutational robustness Might be defined as a function of the mean and variance of the distribution of mutational effects. Environmental robustness Might be defined as ...


1

No. To determine the genetic relationship (if any) between two individuals requires molecular evidence based on genetic markers in their somatic DNA. Using phenotypes could be misleading because a genetic marker (an allele) can have variable penetrance (the percentage of carriers who actually have the phenotype) and variable expressivity (the severity or ...


1

To support mdperry's answer: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2429870/ Figure 2 in particular should draw your attention as it shows the previously mentioned correlation between chromosome size, transcripts and embryonic viability. Apologies, I would have added this in comment form but I do not have enough reputation.



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