Hot answers tagged gene
20
There is a distinct difference between the 'genes' that we share, and the genetic code (the DNA) that the genes are made of.
All humans (excluding genetic disorders) have the same genes, but not everyone has exactly the same code - there are tiny differences between individuals, and these are manifested in the different traits you can observe between people ...
16
In addition to the other answers, let me show you a logical error in your reasoning:
Don't we share 50% of our genes with our mother and 50% with our father?
You get 50% of our genes from each respective parent (disregarding mutations for now). But if you shared only 50% with each parent, this would imply that your parents don’t share a single gene:
...
11
In every cell of your body, you have two physical copies of every gene (ignoring gametes, / copy number variations), one from your mother, one from your father. (Humans are diploid.) That's why it's correct to say that you got 50% from either parent (ignoring the 13 mitochondrial genes that are inherited from the mother only).
The second approach is to ...
11
I know of only one naive approach to determining the boundaries of a gene : RACE-PCR. There are two kinds, 3' and 5' RACE, which allow to find the respective extremities.
The rationale is the following :
You perform a reverse transcription of the transcript of interest using a specific primer. At this step you have a specific single stranded cDNA.
Then ...
8
There are various software in which you can enter your sequence (let's say the whole genome sequence) and it can identify for you the putative open reading frames (ORFs), i.e. the start codons and the stop codons. Then, by using these putative genes, you can do a sequence alignment by using BLAST and then, based on the scores you can confirm that those are ...
7
In short, yes, it is possible. There are companies that sequence part of your genome and then can trace it back to your ancestors. All human family trees can be traced back to their African origin 200 000 years ago, but the companies that sequence your genes do not do that. For example, 23andMe sequences only 1 million of your base pairs (single nucleotide ...
7
In short, because the easiest way to get the protein coding sequence of the gene is to create cDNA based on the mRNA, and insulin mRNA is only expressed in pancreatic cells.
Insulin gene consists of two exons. That means, amplifying the genome will not give us a coding sequence -- two pieces of that sequence will be interrupted by a large, non-coding ...
6
The storage of memories in cells is rarely thought of on the protein level of the cell. Cells are usually given a developmental state, but no memory. A cell may become a liver cell, cancerous, or diabetic, but this is not memory, but a physiological change in the cell which is usually not reversible to a previous state.
For example cancer treatments are ...
6
If your goal is to define the boundaries of the transcription unit (the part of the DNA that is transcribed) the above answer is accurate, although many people merely use homology to cloned cDNAs rather than RACE reactions. This approach has the benefit of defining alternative splice forms at the same time.
If your goal is to define the "ends" of the gene, ...
5
Let's start with a word of caution: on the internet, the terms macroevolution and microevolution (especially together) are usually used primarily in creationist rhetoric. As such, it is usually best to avoid them, especially when talking to a lay audience. The main mistake creationist perpetuate when thinking about micro-vs-macro evolution, is that the two ...
5
Operons, often but not always, contain clusters of genes (under the control of an operator region) which are involved in the same metabolic pathway. There have been several theories for how these groups of genes have arisen but the current feeling seems to be based around the regulation of the genes in question 1. To facilitate co-ordinated gene regulation ...
5
If your goal is to avoid regulatory elements, I would not believe any prediction program, since new regulatory elements are found every day. The best way would be empirical and just clone and infect with a mutated 3'UTR and see if your gene's regulation is perturbed. You could at least swap the entire 3'UTR with that from another gene to see if there are ...
4
Generally speaking you sequence the genome and then search for clues. There are usually specific sequences preceding a gene that help the translational equipment know "hello this is where we begin" as well as regions where proteins can bind that are used to enhance or inhibit translation of the gene.
Computers can be programmed to search through the ...
4
I'd add genetic effects of the gene and its orthologs in that own
host. Knockouts and overexpression are powerful in uncovering
function.
In terms of baseline or normal expression, I would add tissue,
developmental or differentiation time points, and conditions which stimulate or repress expression.
4
There is a useful set of links to nomenclature guidelines for all of the main genetic systems at this Wikipedia page. Personally, I think that the Saccharomyces cerevisiae system works best: it manages to cover dominant and recessive alleles of a gene, the name of the protein, how to refer to a related phenotype, and the use of a parallel convention for the ...
4
That's a good question, and honestly, the nomenclature for genes and their coded proteins is somewhat abused in scientific literature. For example, when referring to microbes (like E. coli), gene names are all lowercase (eg, lacZ). The problem of protein names is compounded when the protein name is (often) an abbreviation.
With respect to myc, it can refer ...
3
This question appears to start from the premise that different species of yeast are closely related, but they aren't. Saccharomyces cerevisae and Schizosaccharomyces pombe, both Ascomycetes, are thought to have diverged at least 300 million years ago (c.f. the mammalian divergence from other vertebrates was about 200 million years ago).
S. cerevisiae has a ...
3
So what is the fuss about?
The fuss isn’t so much about biology as it is about the circumstances of the argument. in particular, I gather that there are two complaints people have with E. O. Wilson’s (and his collaborators’) arguments:
The Wilsonians pretend that kin selection (inclusive fitness) is just a quaint, outdated theory which is trivially ...
3
After reading the article, the fuss is about this:
In currently accepted theory Eusociality or "kin selection" explains altruistic behavior (the sacrifice of yourself or resources you control for the betterment of something else besides you) by relating the act to the amount of genetic information passed on.
B*r > C is the equation I recall, though damned ...
2
Here is an example in which the knockout of a non-essential gene in yeast (Saccharomyces cerevisiae) suppresses the lethal effects of a different knockout.
Amy L. Kistler and Christine Guthrie (2001) Deletion of MUD2, the yeast homolog of U2AF65, can bypass the requirement for Sub2, an essential spliceosomal ATPase. Genes & Development 15:42-49
The ...
2
Strictly speaking no. There are ideas about cultural inheritance though that seem relevant here: see http://www.ncbi.nlm.nih.gov/pubmed/11425279. Cultural inheritance theory uses the plasticity of the human brain as the evidence for the underlying genetics of culture. I.e. we aren't born with the ability to speak English because our parents learned it but ...
2
I think that you could try a similar approach to GSFS:
use transduction in proteins (if you don't know star code, then you must use 3 strings for each gene)
use a basic tool (a stand alone like UNIPROT tools) to identify the proteic domain type (chain alpha, ..)
divide the genes by proteic domain type (pdt): which contains which pdt and the pdt order ...
2
If you're interested in understanding the maintenance of state, history, and information, I would look at hysteresis. The classic biophysics model for studying hysteresis has been the Lambda phage which has been extensively detailed in Mark Ptashne's A Genetic Switch
2
Back when I was doing my PhD, there was a group in the same department as me working on an interesting project exploring the extent to which surnames (generally paternally inherited, at least in the modern west) and Y chromosomes (always paternally inherited) shared their descent.
The answers are always complicated, especially for more common surnames ...
2
There is very interesting work in this regard done by Ed Marcotte. An overview of the "machine" and its conservation across species is here. The point here is the machine or network is conserved, but used in different ways in different organisms. Hence, the phenotypes of mutants might be different, but they'd be consistent across many variants in the ...
2
Perhaps you want to ask how VDJ recombination is regulated in non lymphoid cells..
Well even in immature lymphoid cells VDJ recombination is regulated. And also Ig genes are suppressed in T-cell and TCR genes are suppressed in B-cells..
Also, the recombination of Ig is suppressed in T-cell and vice-versa.
RAG-1,2(Recombination activating gene) ...
1
Another paper from Yamanaka's group explains Fbx15.
It says:
Inactivation of Oct3/4 in ES cells led to rapid extinction of Fbx15 expression.
Fbx15-null ES cells were normal in morphology, proliferation, and differentiation. These data demonstrate that Fbx15 is a novel target of Oct3/4 but is dispensable for ES cell self-renewal, development, and ...
1
Urnov et al. are trying to effect gene therapy - where a mutation causing a genetic form of severe combined immunideficiency (SCID) (also known as the bubble boy syndrome). Affected SCID patients can have little to no immunity to infection what so ever. SCID in this case is caused by a single site mutation in the IL2R-gamma gene.
Their method is to use a ...
Only top voted, non community-wiki answers of a minimum length are eligible
