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Genetics Lecture: Inheritance Patterns, Punnett Squares, and Pedigrees, Study notes of Biology

A lecture note from chapter 12, section 12.3 and 12.4, focusing on patterns of inheritance, punnett squares, and pedigrees in genetics. Topics include mendelian and sex-linked loci, complete and incomplete dominance, codominance, sex-linked characters, epistasis, x-inactivation, and the environment's role in gene expression. Real-life examples are provided for better understanding.

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Lecture 32 11/15/13
Chapter 12 – Section 12.3, 12.4 Friday
Lecture Objectives:
1. Describe patterns of inheritance in Mendelian and sex-linked loci.
2. Use Punnett Squares or pedigrees to determine modes of inheritance.
3. Explain the role of the environment in patterns of expression.
Some traits are inherited as Mendel predicted…some are not.
- Complete /Incomplete dominance
- Co-dominance – blood type
- Sex-linked – orange vs. black cat
- Epistasis/Pleiotropy – Labrador retriever color
- Gene by environment – temperature-sensitive pigment
- Quantitative traits – height
- Linked genes
Pedigrees are used to observe Mendel’s laws.
-Use Punnett squares to predict the potential outcome and ratios of potential phenotypes of
offspring
-We don’t have enough children usually to show those predicted ratios.
-We use pedigrees to look at the actual observations.
oCircle = female
oSquare = male
oWhite doesn’t have phenotype, solid has phenotype.
-Carrier doesn’t’ show up in phenotype (half-filled)
-Dominant shows up in every generation. Recessive stays masked. Until the carrier mates with
another carrier, you may not see the phenotype show b/c its recessive.
- Huntington’s disease = dominant
- Albinism = recessive
Incomplete dominance may be due to many mechanisms.
-Heterozygote has a different phenotype than both of the parents.
-Copy of a gene that codes for a protein that doesn’t function so well.
-Two little aa’s, enzyme can’t work
oPrecursor – some compound in the flower and enzyme doesn’t work (cant convert into
red pigment) so white flower
-Enzyme used in depositing pigment but doesn’t work completely
In codominance, both alleles are expressed equally.
-Different heterozygote but has both alleles expressed equally
-Blood type examples
oOn cell membrane, you have glycoproteins (have sugars attached to them). You have
different glycoproteins on your blood cells. There are four different common blood
types:
A – has A glycoproteins
Can’t accept B
B – different type of glycoprotein
Can’t accept A
AB – A and B glycoproteins
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Download Genetics Lecture: Inheritance Patterns, Punnett Squares, and Pedigrees and more Study notes Biology in PDF only on Docsity!

Chapter 12 – Section 12.3, 12.4 Friday Lecture Objectives:

  1. Describe patterns of inheritance in Mendelian and sex-linked loci.
  2. Use Punnett Squares or pedigrees to determine modes of inheritance.
  3. Explain the role of the environment in patterns of expression. Some traits are inherited as Mendel predicted…some are not.
  • Complete /Incomplete dominance
  • Co-dominance – blood type
  • Sex-linked – orange vs. black cat
  • Epistasis/Pleiotropy – Labrador retriever color
  • Gene by environment – temperature-sensitive pigment
  • Quantitative traits – height
  • Linked genes Pedigrees are used to observe Mendel’s laws.
  • Use Punnett squares to predict the potential outcome and ratios of potential phenotypes of offspring
  • We don’t have enough children usually to show those predicted ratios.
  • We use pedigrees to look at the actual observations. o Circle = female o Square = male o White doesn’t have phenotype, solid has phenotype.
  • Carrier doesn’t’ show up in phenotype (half-filled)
  • Dominant shows up in every generation. Recessive stays masked. Until the carrier mates with another carrier, you may not see the phenotype show b/c its recessive.
  • Huntington’s disease = dominant
  • Albinism = recessive Incomplete dominance may be due to many mechanisms.
  • Heterozygote has a different phenotype than both of the parents.
  • Copy of a gene that codes for a protein that doesn’t function so well.
  • Two little aa’s, enzyme can’t work o Precursor – some compound in the flower and enzyme doesn’t work (cant convert into red pigment) so white flower
  • Enzyme used in depositing pigment but doesn’t work completely In codominance, both alleles are expressed equally.
  • Different heterozygote but has both alleles expressed equally
  • Blood type examples o On cell membrane, you have glycoproteins (have sugars attached to them). You have different glycoproteins on your blood cells. There are four different common blood types:  A – has A glycoproteins  Can’t accept B  B – different type of glycoprotein  Can’t accept A  AB – A and B glycoproteins

Chapter 12 – Section 12.3, 12.4 Friday  No antibodies  Universal acceptor  A and B are codominant to one another  O – no glycoproteins (recessive, no expression of the gene) (ii)  No antigens  Universal donor  Can’t accept A, B, or AB Frizzle fowl are not true-breeding. When crossed, they produce 50% frizzles, 25% normal, and 25% wooly feathers.

  1. What is the genotype of a frizzle chicken? F^N F^W (heterozygote)
  2. How would you explain the mode of inheritance? incomplete dominance Sex-linked characters are on sex chromosomes.
  • XY – male (X is larger than Y)
  • Hemizygous – chromosomes of different sizes when they line up
  • Only one copy of gene in heterogametic sex
  • If you are male, you only have one copy (one allele) for everything on the X chromosomes. The girls have two, however. o Heterogametic sex – have two different chromosomes o Spews our ratios of traits o It shows up more often in the son than you’d expect b/c they only have one.  You can’t mask the traits
  • X^T, X^t, Y (male)
  • If guys function perfectly well with an x and a y, what happens to female with two X’s? o Some are masked (both alleles are expressed, but you see the dominant one) o X-inactivation/Mosaics  One of our chromosomes is completely condensed and shut down so its non- functional in your normal cells.  One of our x’s is off. Which one is random.  Makes you a mosaic of your parents x’s.
  • Red-Green color blind
  • Hemophilia o Dad has recessive X^r, and mom has normal o Daughters get a recessive from dad and dominant from mom, sons get dad’s y and mom’s dominant X o Daughters become carriers but sons aren’t. o Typically, females are carriers and sons are affected more often. In this litter, the female cat has a few orange kittens and some multicolor kittens.
  • Coat color is sex-linked in cats.
  • Black is dominant to orange.
  • Because of X-inactivation, in a female that is heterozygous, she ends up with a tortoise shell pattern (some black and some orange).
  1. What is mom’s genotype?

Chapter 12 – Section 12.3, 12.4 Friday  Expect to grow black patch of hair  Very difficult to confirm on human experiments!! Some allele combinations are lethal.

  • Blood cell shape: N, n
  • nn is lethal when human is an embryo o if you get both copies of those alleles, you get embryonic lethal (die before you’re mature)
  • Nn has normal and sickled cells.
  • NN is normal.
  • If you cross two individuals with sickle cell anemia, what are your phenotypic ratios?
  • Google these others: Gongenital ichthyosis, cystic fibrosis, Huntington’s disease, polydactyly Some traits are quantitative.
  • Not all traits are controlled by one gene.
  • Distribution of people with different heights (controlled by many genes)
  • Quantitative trait loci
  • Genes and environment o How tall you are depends on how well you were fed when you were young (environmental conditions play a role)