Molecular Life Science Review June 15, 2003 Learning objectives- What is sickle cell anemia? Increased knowledge of the structure of atoms, molecules,

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Presentation transcript:

Molecular Life Science Review June 15, 2003 Learning objectives- What is sickle cell anemia? Increased knowledge of the structure of atoms, molecules, and biomolecules Central Dogma How DNA mutations result in abnormal proteins Protein structure classifications How to perform comparisons of protein sequences Workshops- Import cytochrome C sequences of different species. Perform Clustal W comparison Find out the molecular basis of sickle cell anemia

Symptoms of Sickle Cell Anemia pain episodes strokes increased infections leg ulcers bone damage yellow eyes or jaundice early gallstones lung blockage kidney damage and loss of body water in urine painful erections in men (priapism) blood blockage in the spleen or liver (sequestration) eye damage low red blood cell counts (anemia) delayed growth

Hierarchy of particles Atoms (Eg. C, H, O, N) Molecules (Eg. H 2 O, CH 4 ) small Biomolecules (Eg. Sugars, amino acids) large Biomolecules (Eg. polysacharrides, proteins)

Example of ionic bond

H + H  H 2 O + O  O 2 2H 2 O  2H 2 + O 2 Chemical Reactions

Covalent Bonds (electrons shared)

pH scale. A convenient method to measure the concentration of H + pH = -log[H + ] Remember pH + pOH = 14 M = 1 mole/liter

Amino acid characteristics

Website for Amino acid interactive Workshop Amino acids 1 2

DNA sequence Write the primary sequence of the DNA displayed in 3B Molecular_Graphics/DNA_Str ucture/DNA_Tutorial.HTML Molecular_Graphics/DNA_Str ucture/DNA_Tutorial.HTML rc.ac.uk/notebook/courses/g uide/dnast.htm rc.ac.uk/notebook/courses/g uide/dnast.htm Website for interactive workshop for DNA analysis

Interactive display of amino acid and codons

Translation exercise Translate the following sequence using the codon table: ATGGUGCACCUGACUCCUGAGGAGAAG Perform same procedure using a software program:

Central Dogma DNA RNA Protein

DNA RNA (with ribosomes)

*

>gi| |gb|AAA | p53 tumor suppressor homolog MSQGTSPNSQETFNLLWDSLEQVTANEYTQIHERGVGYEYHEAEPDQTSLEISAYRIAQPDPYGRSESYD LLNPIINQIPAPMPIADTQNNPLVNHCPYEDMPVSSTPYSPHDHVQSPQPSVPSNIKYPGEYVFEMSFAQ PSKETKSTTWTYSEKLDKLYVRMATTCPVRFKTARPPPSGCQIRAMPIYMKPEHVQEVVKRCPNHATAKE HNEKHPAPLHIVRCEHKLAKYHEDKYSGRQSVLIPHEMPQAGSEWVVNLYQFMCLGSCVGGPNRRPIQLV FTLEKDNQVLGRRAVEVRICACPGRDRKADEKASLVSKPPSPKKNGFPQRSLVLTNDITKITPKKRKIDD ECFTLKVRGRENYEILCKLRDIMELAARIPEAERLLYKQERQAPIGRLTSLPSSSSNGSQDGSRSSTAFS TSDSSQVNSSQNNTQMVNGQVPHEEETPVTKCEPTENTIAQWLTKLGLQAYIDNFQQKGLHNMFQLDEFT LEDLQSMRIGTGHRNKIWKSLLDYRRLLSSGTESQALQHAASNASTLSVGSQNSYCPGFYEVTRYTYKHT ISYL FASTA format

Multiple sequence alignment Human-locus number AAA35732 Dog-locus number CCDG Yeast-locus number from structure or protein sequence database 1YCC CLUSTAL PROGRAM

Workshop Find out the chromosomal location of the gene that causes sickle cell anemia. Give the name of the gene. Find out the nucleotide change and amino acid change that leads to sickle cell anemia (there may be more than one change that gives rise to the disease) If sickle cell anemia is so devastating, why has it lasted in the population for such a long time? Give a molecular explanation (you may have to do a little research to get this) Print out answers and show instructor.