Cloning Issue : * What are some of the social challenges a cloned child might face?

As all of us know, cloning might result in either longer chromosome or shorter chromosome. Both of them are not good for any cloned organism to have. Shorter chromosome will cause the organism going through aging faster at a faster rate, and longer chromosome will cause the organism going at a slower rate. Not one of those can make the cloned children avoid social challenge they will meet in the future.

Let's say for a children with shorter chromosome, which will cause them to aging at a faster rate than common children. As an adult or parents, we don't want to see those children to face embarrassment from their friends. Those children might be bigger in face or have an older face, but brain-wise, they are no more than children at their age. That embarrassment might cause a deep pressure for the children. On the other hand, longer chromosome is not better than shorter chromosome. Longer chromosome, too, will cause embarrassment for the children in a different way. As it will aging slower, the cloned children, even though have the same level of education and equal in intelligent, they are smaller in size and younger in face. Both defects of chromosome that common in a cloned organism will cause social challenge that cloned children have to face, they can't avoid those problems.

Actually, there is more than social challenge, cloned organism might also suffer from health challenges that have chance to kill them. How if, in the cloning process, an error happened in the cell differentiation process? Isn't it will cause a serious health problem that the child have to face?
Cloning has serious risks that the cloned organisms themselves have to bear, not the researcher nor the creator. Both social and health problems will cause unavoidable challenges that they have to face.

Transcription, Translation, and Protein Synthesis

Transcription is the process in which RNA copy the sequence of DNA. First of all the DNA unzipped, promotor attached, then RNA synthesis at the promotor, and finally DNA zips back up.

Translation is a process in which RNA language is translated into DNA language. The first thing that happened is amino acid attached to tRNA. Then, tRNA attached to ribosomes and later on attached to the mRNA. Next thing that happened is another tRNA comes in and repeat until they make a single RNA, which is the exact copy of the original DNA.

Last but not least is protein synthesis. Protein synthesis is basically meaning the building of protein starting from amino acid, which is the basic single unit of protein, just like carbohydrate is composed of a lot of monosaccharides.

Nucleotide BLAST! Gene sequence and summary

Gene 2

Gene sequence 2:

ATG GCG GGT CTG ACG GCG GCG GCC CCG CGG CCC GGA GTC CTC CTG CTC CTG CTG TCC ATC CTC CAC
CCC TCT CGG CCT GGA GGG GTC CCT GGG GCC ATT CCT GGT GGA GTT CCT GGA GGA GTC TT

Gene 2 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

Gene sequence 3:

ATG CTC ACA TTC ATG GCC TCT GAC AGC GAG GAA GAA GTG TGT GAT GAG CGG ACG TCC CTA ATG TCG
GCC GAG AGC CCC AGC CCG CGC TCC TGC CAG GAG GGC AGG CAG GGC CCA GAG GAT GGA G

Gene 3 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 5

Gene sequence 5:

ATG CGT CGA GGG CGT CTG CTG GAG ATC GCC CTG GGA TTT ACC GTG CTT TTA GCG TCC TAC ACG AGC
CAT GGG GCG GAC GCC AAT TTG GAG GCT GGG AAC GTG AAG GAA ACC AGA GCC AGT CGG GCC

Gene 5 summary:

This gene encodes a member of the fibrillin family. The encoded protein is a large, extracellular matrix glycoprotein that serve as a structural component of 10-12 nm calcium-binding microfibrils. These microfibrils provide force bearing structural support in elastic and nonelastic connective tissue throughout the body. Mutations in this gene are associated with Marfan syndrome, isolated ectopia lentis, autosomal dominant Weill-Marchesani syndrome, MASS syndrome, and Shprintzen-Goldberg craniosynostosis syndrome. [provided by RefSeq, Jul 2008]

Gene 6

Gene sequence 6:

ATG CCG CCC AAA ACC CCC CGA AAA ACG GCC GCC ACC GCC GCC GCT GCC GCC GCG GAA CCC GGC ACC
GCC GCC GCC GCC CCC TCC TGA GGG ACC CAG AGC AGG ACA GCG GCC CGG AGG AC

Gene 6 summary:

The protein encoded by this gene is a negative regulator of the cell cycle and was the first tumor suppressor gene found. The encoded protein also stabilizes constitutive heterochromatin to maintain the overall chromatin structure. The active, hypophosphorylated form of the protein binds transcription factor E2F1. Defects in this gene are a cause of childhood cancer retinoblastoma (RB), bladder cancer, and osteogenic sarcoma. [provided by RefSeq, Jul 2008]