cloning questions.

What are some of the social challenges a cloned child might face?
A cloned child may encounter a lot of negativity. They might get bullied, whether verbally or non-verbally. The cloned child may be an outcast. Other people will tease and talk about them a lot. People will tease them about lacking originality and how they are cloned. People who disapprove of cloning greatly may abuse the cloned child, so the cloned child's life could be at risk too.

Should cloning research be regulated? How, and by whom? (extra credit)
Cloning research should not be regulated. We should continue researching cloning that will benefit our society. Research on cloning plants, etc is acceptable because that could benefit our agriculture market. Research on cloning humans, etc should be regulated. The country should ban research on cloning and give consequences to whoever disobeys the law.

references: http://learn.genetics.utah.edu/content/tech/cloning/whatiscloning/

different types of mutations.

Sense Mutation: a single substitution mutation when the change in the DNA base sequence results in a new codon still coding for the same amino acid 

Non-sense Mutation: a codon that stands for an amino acid mutates to one of these three stop codons. Nonsense mutations cause the protein to be cut off early and therefore incomplete, which usually renders it non-functional.

Deletion Mutation: A type of gene mutation wherein the deletion (as well as addition) of (a number of) nucleotide(s) causes a shift in the reading frame of the codons in the mRNA, thus, may eventually lead to the alteration in the amino acid sequence at protein translation. 

Insertion Mutation: A type of mutation resulting from the addition of extra nucleotides in a DNA sequence or chromosome. Insertion of a larger segment into the chromosome can also lead to mutation. It results when an unequal crossover happens during meiosis. 

Frameshift Mutation: A mutation seen when a number of DNA nucleotides not divisible by three is added or deleted. This causes a reading frame shift and all of the codons and all of the amino acids after that mutation are usually wrong. 

Point Mutation:  A mutation in DNA or RNA molecule involving a change of only one nucleotide base. It is a simple change in one base of the gene sequence.

Translocation Mutation: Translocations are the transfer of a piece of one chromosome to a nonhomologous chromosome. Translocations are often reciprocal; that is, the two nonhomologues swap segments. 

 references: http://www.biology-online.org http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/M/Mutations.html http://www.genetichealth.com/g101_changes_in_dna.shtml

transcription, translation

Transcription: Transcription is the process of creating a complementary RNA copy of a sequence of DNA. Both RNA and DNA are nucleic acids, which use base pairs of nucleotides as a complementary language that can be converted back and forth from DNA to RNA by the action of the correct enzymes. During transcription, a DNA sequence is read by an RNA polymerase, which produces a complementary, antiparallel RNA strand. As opposed to DNA replication, transcription results in an RNA complement that includes uracil (U) in all instances where thymine (T) would have occurred in a DNA complement.

Translation:  In molecular biology and genetics, translation is the third stage of protein biosynthesis (part of the overall process of gene expression). In translation, messenger RNA (mRNA) produced by transcription is decoded by the ribosome to produce a specific amino acid chain, or polypeptide, that will later fold into an active protein. In Bacteria, translation occurs in the cell's cytoplasm, where the large and small subunits of the ribosome are located, and bind to the mRNA. In Eukaryotes, translation occurs across the membrane of the endoplasmic reticulum in a process called vectorial synthesis. The ribosome facilitates decoding by inducing the binding of tRNAs with complementary anticodon sequences to that of the mRNA. The tRNAs carry specific amino acids that are chained together into a polypeptide as the mRNA passes through and is "read" by the ribosome in a fashion reminiscent to that of a stock ticker and ticker tape.

references: http://en.wikipedia.org/wiki/Translation_%28biology%29

http://en.wikipedia.org/wiki/Transcription_%28genetics%29

name that gene.

Gene 1: 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.
Gene 2: 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.
Gene3: 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.
Gene4:  Cystic fibrosis is a disease passed down through families that causes thick, sticky mucus to build up in the lungs, digestive tract, and other areas of the body. It is one of the most common chronic lung diseases in children and young adults. It is a life-threatening disorder.
Gene5:  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.
Gene6:  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.
Gene7:  ATP7A is important for regulating copper levels in the body. This protein is found in most tissues, but it is absent from the liver. In the small intestine, the ATP7A protein helps control the absorption of copper from food. In other organs and tissues, the ATP7A protein has a dual role and shuttles between two locations within the cell. The protein normally resides in a cell structure called the Golgi apparatus, which modifies and transports newly produced enzymes and other proteins. Here, the ATP7A protein supplies copper to certain enzymes that are critical for the structure and function of bone, skin, hair, blood vessels, and the nervous system. If copper levels in the cell environment are elevated, however, the ATP7A protein moves to the cell membrane and eliminates excess copper from the cell.
Gene8:  The dystrophin gene is the largest gene found in nature, measuring 2.4 Mb. The gene was identified through a positional cloning approach, targeted at the isolation of the gene responsible for Duchenne (DMD) and Becker (BMD) Muscular Dystrophies. DMD is a recessive, fatal, X-linked disorder occurring at a frequency of about 1 in 3,500 new-born males. BMD is a milder allelic form. In general, DMD patients carry mutations which cause premature translation termination (nonsense or frame shift mutations), while in BMD patients dystrophin is reduced either in molecular weight (derived from in-frame deletions) or in expression level. The dystrophin gene is highly complex, containing at least eight independent, tissue-specific promoters and two polyA-addition sites. Furthermore, dystrophin RNA is differentially spliced, producing a range of different transcripts, encoding a large set of protein isoforms. Dystrophin (as encoded by the Dp427 transcripts) is a large, rod-like cytoskeletal protein which is found at the inner surface of muscle fibers. Dystrophin is part of the dystrophin-glycoprotein complex (DGC), which bridges the inner cytoskeleton (F-actin) and the extra-cellular matrix.

references: http://blast.ncbi.nlm.nih.gov/Blast.cgi?PROGRAM=blastn&BLAST_PROGRAMS=megaBlast&PAGE_TYPE=BlastSearch&SHOW_DEFAULTS=on&LINK_LOC=blasthome
http://www.biologycorner.com/worksheets/name_that_gene.html