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LET’S PUT SOME ALLELES ON SOME CHROMOSOMES

LET’S PUT SOME ALLELES ON SOME CHROMOSOMES. T= Allele for “curled tongue” t= Allele for “flat” tongue” . T. t. l. L. L= Allele for ear lobe l= Allele for attached ear lobe . Can you figure out how MEIOSIS Does this???. P 1 TtLl Curled Tongue & Lobed Ears.

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LET’S PUT SOME ALLELES ON SOME CHROMOSOMES

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  1. LET’S PUT SOME ALLELES ON SOME CHROMOSOMES T= Allele for “curled tongue” t= Allele for “flat” tongue” T t l L L= Allele for ear lobe l= Allele for attached ear lobe

  2. Can you figure out how MEIOSIS Does this??? P1 TtLl Curled Tongue & Lobed Ears What are the Gametes??? TL Tl tL tl

  3. T t l L tL Tl

  4. But, there is an equal chance (50/50) that the pairs of homologous chromosomes may line up on either side of the cell.

  5. T t L l tl TL

  6. You should be able to figure out how MEIOSIS results in all 4 possible combinations of alleles. P1 TtLl Curled Tongue & Lobed Ears Gametes??? TL Tl tL tl

  7. Human Genetics Some Important terms: 1. Dominant (tall peas) 2. Recessive (short peas) 3. Homozygous dominant TT Homozygous recessive tt 4. Heterozygous Tt 5. Gene 6. Allele 7. Homologous Chromosomes 8. Linkage (many genes on the same chromosome) 9. Crossing over (exchanges within chromosomes) 10. Phenotype What we express (Tall Pea) 11. Genotype What’s in our DNA (Tt)

  8. Some Human traits are the result of A Recessive Allele…. They only show up when the individual is homozygous recessive. Example: ALBINISM The most commom form of ALBINISM Is caused by a defect in a key enzyme-Tyrosinase, the enzyme that make a precursor for the production of the pigment molecule: MELANIN

  9. ALBINISM (ALLELES) A= NORMAL PIGMENTATION a= ALBINISM What about an individual who is HETEROZYGOUS Aa ?? Can you describe this using the terms Transcription and translation?

  10. ALBINISM HETEROZYGOUS person Aa Has NORMAL pigmentation. Q. WHY? A. The 1 copy of the Allele “A” is able to produce enough of the enzyme TYROSINASE to make the precursor and to allow melanin synthesis to proceed.

  11. ALBINISM SO---the only way to have this trait show up is to have 2 copies of the recessive allele (a) that is unable to code for a working copy of the enzyme tyrosinase, in other words, to be: Homozygous recessive aa

  12. Some Human traits, however, are the caused by DOMINANT alleles--- That means that if you get just ONE COPY of the allele, you will show the trait An example is Huntington’s Disease, a brain disease. HH= Huntington’sDisease Hh= Huntington’sDisease hh= Normal

  13. Text Fig. 7.28 A Dominant Trait: Huntington’s Disease

  14. Genetics and Human Diseases

  15. Down Syndrome TRISOMY-21 A Chromosome-based Human genetic disorder

  16. Text Fig. 7.19 Human Karyotype

  17. Text Fig. 7.20 Down Syndrome

  18. Text Fig. 7.22 Nondisjunction Of the X chromosome Chromosomes Pair in the Forming egg, But they don’t Separate...

  19. Text Fig. 7.21 Mother’s Age And Down syndrome

  20. Text Fig. 7.29 Amniocentesis

  21. Text Fig. 7.14 MULTIPLE GENES: Height MOST HUMAN TRAITS ARE REGULATED BY SEVERAL DIFFERENT GENES…TRAITS SUCH AS HEIGHT AND SKIN COLOR.

  22. SOME HUMAN TRAITS ARE REGULATED BY A SINGLE GENE… BUT IN THE HUMAN POPULATION THERE MAY BE MORE THAN TWO DIFFERENT ALLELES FOR THE GENE. AN EXAMPLE IS BLOOD GROUPS… TYPE A TYPE B TYPE O

  23. MULTIPLE ALLELES HUMAN BLOOD GROUPS THE BLOOD CELLS HAVE A MARKER ON THE CELL SURFACE THAT MAY BE A TYPE “A” OR “B” ANTIGEN… OR THERE MAY BE NO ANTIGEN (“O”) ON THE CELL SURFACE. ITHERE ARE 3 DIFFERENT IAALLELES, BUT A PERSON IBCAN ONLY HAVE 2 OF THEM

  24. IA I = TYPE A IA IA = TYPE A IA IB = TYPE AB IB I= TYPE B IB IB = TYPE B I I = TYPE O

  25. Text Fig. 7.13 Multiple Alleles Blood Groups

  26. PARENTS: Type A X Type B CHILD TYPE AB IA IA X IB IB IA IB IAIB

  27. PROBLEM: MOTHER TYPE A CHILD TYPE O COULD FATHER BE TYPE B?? COULD FATHER BE TYPE A? COULD FATHER BE TYPE O?

  28. IA I = TYPE A IA IA = TYPE A IB I= TYPE B IB IB = TYPE B I I = TYPE O

  29. PROBLEM: MOTHER TYPE A ( IA IA OR IA I ) CHILD TYPE O (ONLY I I) COULD FATHER BE TYPE B?? (YES, IA I) COULD FATHER BE TYPE A? (YES, IAI) COULD FATHER BE TYPE O? (YES, I I)

  30. SICKLE CELL A disease of Red Blood Cells A disease of the protein Hemoglobin The affected Red Blood Cells do not carry Oxygen as well as normal Red Blood Cells

  31. SICKLE CELL A disease of Red Blood Cells NORMAL HbA HbA SICKLE CELL TRAIT HbA HbS SICKLE CELL DISEASE HbS HbS

  32. The beta (b) polypeptide of Hemoglobin has 146Amino Acids. The normalHbA polypeptide has the amino acid glutamic acid (1 of 20)in the number 6 position: AA-AA-AA-AA-AA-GLUTAMIC ACID-AA-AA- The Sickle CellHbS polypeptide has the wrong amino acid at position # 6, a valine rather than a glutamic acid. AA-AA-AA-AA-AA-Valine-AA-AA-

  33. The DNA code for Glutamic acid (HbA) is -CTC- The DNA code for valine (HbS) is -CAC- DNA IN THE Hb gene -------CTC---- NORMAL (HbA) OR -------CAC---- SICKLE CELL (HbS)

  34. Text. Fig. 7.25 Sickled Red Blood Cells

  35. Text Table 7.2 Human Genetic Disorders

  36. PKU is an “Inborn Error of Metabolism” The condition results from the lack of a key enzyme in thae pathway that breaks down Excess phenylalanine,one of the essential amino acids. In the absence of the enzyme, excess Phenylalanine is converted into a toxin, resulting in brain damage. Sceening at birth for PKU is now standard, and children can be put onto a diet with Phenylalanine restricted to just the amound needed for protein synthesis.

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