Mendelian genetics and punnett squares

Last updated: February 24, 2023

Mendelian genetics and punnett squares

POM

POM

Gluconeogenesis
Glycogen metabolism
Amino acid metabolism
Fatty acid synthesis
Fatty acid oxidation
Ketone body metabolism
Cholesterol metabolism
Carbohydrates and sugars
Fats and lipids
Proteins
Cellular structure and function
Cell membrane
Selective permeability of the cell membrane
Extracellular matrix
Cell-cell junctions
Endocytosis and exocytosis
Osmosis
Resting membrane potential
Nernst equation
Cell signaling pathways
Cytoskeleton and intracellular motility
Nuclear structure
DNA structure
Transcription of DNA
Translation of mRNA
Amino acids and protein folding
Protein structure and synthesis
Nucleotide metabolism
DNA replication
Lac operon
DNA damage and repair
Cell cycle
Mitosis and meiosis
DNA mutations
Polymerase chain reaction (PCR) and reverse-transcriptase PCR (RT-PCR)
Gel electrophoresis and genetic testing
ELISA (Enzyme-linked immunosorbent assay)
Karyotyping
DNA cloning
Fluorescence in situ hybridization
Mendelian genetics and punnett squares
Hardy-Weinberg equilibrium
Inheritance patterns
Independent assortment of genes and linkage
Gene regulation
Epigenetics
Evolution and natural selection
Bacterial structure and functions
Free radicals and cellular injury
Necrosis and apoptosis
Ischemia
Hypoxia
Inflammation
Atrophy, aplasia, and hypoplasia
Hyperplasia and hypertrophy
Metaplasia and dysplasia
Oncogenes and tumor suppressor genes
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Thrombolytics
Blood histology
Blood components
Blood groups and transfusions
Platelet plug formation (primary hemostasis)
Coagulation (secondary hemostasis)
Role of Vitamin K in coagulation
Clot retraction and fibrinolysis
Iron deficiency anemia
Beta-thalassemia
Alpha-thalassemia
Sideroblastic anemia
Anemia of chronic disease
Lead poisoning
Hemolytic disease of the newborn
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Autoimmune hemolytic anemia
Pyruvate kinase deficiency
Paroxysmal nocturnal hemoglobinuria
Sickle cell disease (NORD)
Hereditary spherocytosis
Aplastic anemia
Fanconi anemia
Megaloblastic anemia
Diamond-Blackfan anemia
Chronic leukemia
Acute leukemia
Microcytic anemia: Pathology review
Non-hemolytic normocytic anemia: Pathology review
Intrinsic hemolytic normocytic anemia: Pathology review
Extrinsic hemolytic normocytic anemia: Pathology review
Macrocytic anemia: Pathology review
Heme synthesis disorders: Pathology review
Coagulation disorders: Pathology review
Platelet disorders: Pathology review
Mixed platelet and coagulation disorders: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
Lymphomas: Pathology review
Leukemias: Pathology review
Plasma cell disorders: Pathology review
Myeloproliferative disorders: Pathology review
Thymus histology
Spleen histology
Lymph node histology
Introduction to the immune system
Cytokines
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Somatic hypermutation and affinity maturation
VDJ rearrangement
Contracting the immune response and peripheral tolerance
B- and T-cell memory
Anergy, exhaustion, and clonal deletion
Vaccinations
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity

Transcript

Watch video only

Genetics is the science that studies inheritance, or the way parents transmit certain traits to their descendants.

And Mendelian genetics, refers to Gregor Mendel—an Austrian monk—who studied inheritance by experimenting on pea plants.

He cross-pollinated the flowers of different plants together, took the seeds the developed from the pairing, planted those seeds, and took careful notes on the types of peas that resulted in the subsequent generations. As a monk he was just trying to find his inner peas (peace)!

Now in addition to having lots and lots of peas in his garden, he helped to formulate two important laws; the law of segregation and the law of independent assortment.

So to start out - Mendel took plants with violet flowers and plants with white flowers and crossbreed them.

This original group of flowers are called the P generation, as in “parent,” and then when he obtained some peas, he planted them and got more plants and the flowers in this offspring generation was called F1, or filial one.

It turned out that the F1 generation consisted of all violet flowers, so he called the violet trait “dominant,” while the white trait which appeared to be lost in the F1 generation, was called “recessive.”

Next, Mendel let the violet flowers in the F1 generation cross-pollinate amongst themselves, and when they formed peas - he planted them again.

He got more plants and the flowers from that second generation of plants he called filial two or F2.

It turned out that some of the plants in this F2 generation had white flowers whereas other plants had purple flowers! In fact, the ratio was about 3 violet flowering plants for every 1 white flowering plant.

Based on this experiment, Mendel drew a few conclusions.

First, since the F1 violet flowers had some offspring plants that produced violet flowers and other offspring plants that produced white flowers, it meant that the F1 plants must have contained both of these elements.

The inheritable elements of pea plants are its the gametes, so that meant that the gametes of the F1 plant, contained either the dominant violet trait or the recessive white trait.

The F2 plants are created with one gamete from each parent.

And Mendel worked out that the white flowering plants resulted when they receive both white flower elements, and that plants that had at least one violet flower element from either parent would produce violet flowers.

Mendel didn’t know this at the time, but the “element” he was referring to were segments of DNA called genes that encoded flower color.

These genes were located on specific parts of chromosomes, called loci.

Different versions of a gene are called alleles, and in the case of the flowers there were two alleles - a white and violet allele for flower color.

A helpful way to visualize Mendel’s experiment is to use a Punnett square.

Imagine a box with four squares within in, were we put the genetic information of one parent—or genotype—on the horizontal row and the other parent on the vertical column.

The dominant allele, represented with a capital letter, codes for a violet flower; and the recessive allele, represented with a lowercase letter, codes for a white flower.

The letter we choose doesn’t matter, so let’s use capital P for the violet flower allele, and a lowercase p for the white flower allele.

In the P generation Mendel used pure-breeding plants, so their genotype was two of the same alleles.

In other words, both of the parent plants in this generation were homozygous for flower color trait.

“Homo” meaning same, and zygous referring to the male and female alleles.

The violet pea plant had two of the same dominant alleles “PP”, and therefore had all violet flowers, whereas the white pea plant had two of the same recessive alleles “pp”, and therefore had all white flowers.

Key Takeaways

Mendelian genetics is the study of how genes are passed from parents to their offspring. Genes are inherited in pairs, one gene from each parent. Punnett squares are a tool used by geneticists to predict the possible combinations of genes that could be inherited from a particular mating. To use a Punnett square, you first need to determine the genotypes of each parent. Then you can use the Punnett square to predict the possible genotypes of their offspring.