Natural Selection

Natural Selection is a process by which become either more or less common in a function of differential reproduction of their bearers. The mutations do occur to produce brand new alleles that improve organisms chances of survival in a particular environment. Natural selection never affects the genotypes since it is already fixed the genotype combination can never be altered.

Should cloning research be regulated?

My opinion: I think cloning research shouldn't be regulated because cloning can be harmful to the world.

different types of mutations

NONSENSE MUTATIONS: a nonsense mutation, the new nucleotide changes a codon that specified an amino acid to one of the stop codons (TAA, TAG, or TGA). Therefore, translation of the messenger RNA transcribed from this mutant gene will stop prematurely. The earlier in the gene that this occurs, the more truncated the protein product and the more likely that it will be unable to function.

INSERTION: occur when extra DNA is added into an existing gene


FRAMESHIFT:

mutations result from either addition or deletion of one or two nucleotide bases. When this occurs the reading frame is changed so that all the codons read after the mutation are incorrect, even though the bases themselves may be still present.

POINT MUTATIONS: are small changes often in a single nucleotide base.

TRANSLOCATIONS: are the transfer of a piece of one chromosome to a nonhomolougus chromosomes. Translocations are often reciprocal; that is, the two nonhomologues swap 

• the break may occur within a gene destroying its function
• translocated genes may come under the influence of different promoters and enhancers so that their expression is altered. 
• the breakpoint may occur within a gene creating a hybrid gene. This may be transcribed and translated into a protein with an N-terminal of one normal cell protein coupled to the C-terminal of another. The Philadelphia chromosome found so often in the leukemic cells of patients with  (CML) is the result of a translocation which produces a compound gene (bcr-abl).

SENSE MUTATIONS:A mutation that changes a termination  codon into one that codes for an amino acid. Such a mutation results in an elongated protein. 

DELETION MUTATIONS: result in missing DNA are called deletions. These can be small, such as the removal of just one "word," or longer deletions that affect a large number of genes on the chromosome. Deletions can also cause frameshift mutations. In this example, the deletion eliminated the word cat.

transcription, translation

transcription is the synthesis of RNA from a DNA template the concept of transcription wheather prokaryoticor eukaryotic has 3 main events: initian, elongation, termination

translation is the process where m RNA molecules are translated into proteins at the ribosomes

name that Gene

Gene 1:Official Symbol

HTTprovided by HGNC

Official Full Name

huntingtinprovided by HGNC

Primary source

HGNC:4851

See related

Ensembl:ENSG00000197386; HPRD:00883; MIM:613004; Vega:OTTHUMG00000159916

Gene type

protein coding

RefSeq status

REVIEWED

Organism

Homo sapiens

Lineage

Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo

Also known as

HD; IT15

Summary

Huntingtin is a disease gene linked to Huntington's disease, a neurodegenerative disorder characterized by loss of striatal neurons. This is thought to be caused by an expanded, unstable trinucleotide repeat in the huntingtin gene, which translates as a polyglutamine repeat in the protein product. A fairly broad range in the number of trinucleotide repeats has been identified in normal controls, and repeat numbers in excess of 40 have been described as pathological. The huntingtin locus is large, spanning 180 kb and consisting of 67 exons. The huntingtin gene is widely expressed and is required for normal development. It is expressed as 2 alternatively polyadenylated forms displaying different relative abundance in various fetal and adult tissues. The larger transcript is approximately 13.7 kb and is expressed predominantly in adult and fetal brain whereas the smaller transcript of approximately 10.3 kb is more widely expressed. The genetic defect leading to Huntington's disease may not necessarily eliminate transcription, but may confer a new property on the mRNA or alter the function of the protein. One candidate is the huntingtin-associated protein-1, highly expressed in brain, which has increased affinity for huntingtin protein with expanded polyglutamine repeats. This gene contains an upstream open reading frame in the 5' UTR that inhibits expression of the huntingtin gene product through translational repression. [provided by RefSeq, Jul 2008]

Gene 2:

Official Symbol

ELNprovided by HGNC

Official Full Name

elastinprovided by HGNC

Primary source

HGNC:3327

See related

Ensembl:ENSG00000049540; HPRD:00556; MIM:130160; Vega:OTTHUMG00000150229

Gene type

protein coding

RefSeq status

REVIEWED

Organism

Homo sapiens

Lineage

Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo

Also known as

WS; WBS; SVAS

Summary

This gene encodes a protein that is one of the two components of elastic fibers. The encoded protein is rich in hydrophobic amino acids such as glycine and proline, which form mobile hydrophobic regions bounded by crosslinks between lysine residues. Deletions and mutations in this gene are associated with supravalvular aortic stenosis (SVAS) and autosomal dominant cutis laxa. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]

Gene 3:

Official Symbol

PSEN2provided by HGNC

Official Full Name

presenilin 2 (Alzheimer disease 4)provided by HGNC

Primary source

HGNC:9509

See related

Ensembl:ENSG00000143801; HPRD:02860; MIM:600759; Vega:OTTHUMG00000037563

Gene type

protein coding

RefSeq status

REVIEWED

Organism

Homo sapiens

Lineage

Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo

Also known as

AD4; PS2; AD3L; STM2; CMD1V

Summary

Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1 or PSEN2) or the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor such that, they either directly regulate gamma-secretase activity, or themselves act are protease enzymes. Two alternatively spliced transcript variants encoding different isoforms of PSEN2 have been identified. [provided by RefSeq, Jul 2008]

Gene 4:

GDS3489 record | GPL7430 hHR029307 [Homo sapiens]

4 samples Profile Neighbors, Links

Annotation:	Homo sapiens chromosome 7 genomic contig, alternate assembly (based on CRA_TCAGchr7v2)
Reporter:	NT_079596.1 392781 (orf)
Experiment:	CD133 depletion effect on metastatic melanoma cell line, Expression profiling by array, transformed count