Move aside Mendel! Life isn’t all peas and carrots and some rules are made to be broken. Episode 65 recaps several patterns of non-Mendelian inheritance...
Move aside Mendel! Life isn’t all peas and carrots and some rules are made to be broken. Episode 65 recaps several patterns of non-Mendelian inheritance including incomplete dominance (1:59), multiple alleles and codominance (3:21), sex linked recessive traits (5:41), recombinants (7:14) and polygenetic traits (8:14). Get ready to practice your Punnett squares!
The Question of the Day asks (9:39) What organism did Sir Thomas Hunt Morgan perform genetic experiments on while developing his chromosomal theory of inheritance?
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Hi and welcome to the APsolute Recap: Biology Edition. Today’s episode will recap Breaking Mendel’s Rules
Zoom out:
Unit 5 - Heredity
Topic - 5.4
Big idea - Information Storage and Transmission
For as long as I can remember, 2 + 2 equals 4. Gravity makes objects fall and water is wet. The simple reliable things in life. Gregor Mendel enjoyed the reliable as well - purple flowers were dominant to white flowers, and the F2 generation shows a 3:1 ratio. Well move aside Mendel - because life isn’t all peas and carrots and some rules are made to be broken. In today’s episode, 2 + 2 can equal 5, or 6, or maybe even a little bit of both! Genetically speaking at least.
Let’s Zoom in:
We are going to work through some practice problems in each example - so get some scratch paper ready or download our study guide. Even though these are different scenarios, the same process of completing Punnett squares, foiling for gametes in dihybrid cross, and rules of probability still apply. The primary difference in non-Mendelian genetics will be how we interpret genotypic and phenotypic ratios of offspring. As for alleles, there are conventional ways for writing these types of problems, so as to distinguish them from standard dominance scenarios - but so long as you interpret the results correctly, you can write them however you want. (Shhh...Don’t tell your teachers I said that).
First up, incomplete dominance - which is exactly how it's described. Neither allele is fully dominant over the other, and so both are partially expressed when present. Consider the snapdragon flower where capital C superscript R is red and capital C superscript W is white. (C for the color trait and respective letters for each allele variety). A C superscript R homozygous flower is phenotypically red and a C superscript W homozygous flower is white. But a CR CW heterozygous flower exhibits an entirely new intermediate phenotype - pink. Complete a heterozygous cross to show how 50% of the offspring will be pink. Each allele assorts independently just as Mendel predicted, but there is not your standard 3/1 phenotypic ratio in the offspring. Instead, there is 1 red: 2 pink: 1 white. Another example of incomplete dominance is with sickle cell anemia. A heterozygous individual has sickle cell trait, with some cells normally shaped and others sickle shaped. Sickle cell anemia is also a great example of evolution within humans, as sickle cell trait provides malaria resistance in certain environments.
Next, multiple alleles and codominance - time for blood typing! There are three alleles in the population that control the foundation of your blood type, allele A, B and O. Even though there are three alleles, you can still only inherit two! (two parents, homologous chromosomes). A and B are codominant over the recessive allele O. By convention, Capital I’s with superscripts for A or B are used to show their dominance, whereas a lowercase i is used to represent allele o. Considering all combinations, there are four primary phenotypes. Blood type A (expressed as homozygous or heterozygous with a recessive o). Blood type B (same pattern), Blood type AB, and blood type o. Each blood type will dictate different antigens expressed on the cell and antibodies in the plasma to distinguish self from non-self. Let’s practice, show a punnett square that produces all four blood types from a single cross. Need a challenge? Consider adding the Rhesus factor in a new dihybrid cross problem. The Rhesus factor is an additional antigen, which is how we have blood types such as AB+ or O-.
King Henry the 8th, to six wives he was wedded, one died, one survived, two divorced, and two beheaded. I hate to break it to you Henry, but you need to pass on the y chromosome to get that son. In humans, females are genetically XX whereas males are genetically XY. The y chromosome, although very small, contains the SRY gene which leads to the development of male characteristics, like testes. It should be noted that some other species have sex determination with different chromosomes - like ZW in birds and haplodiploidy in bees. Sex-linked traits follow unique patterns. The overwhelming majority of sex-linked traits, and often disorders in genetics problems, are located on the X chromsome and are recessive. Consider red-green colorblindness, a sex linked recessive disorder. A colorblind father and normal mother have children, all of which have normal vision. However, one of their daughters grows up to have a son, who is colorblind. Why? The father passed his affected x chromosome to his daughter, who was then a carrier. When she had a son, there was a 50% chance of passing on the color blind chromosome. Since males only have one X chromosome (called hemizygous), they will express the trait if inherited. For this reason, sex linked recesive disorders are more common in men and often pass from unaffected mothers to affected sons in pedigrees.
The patterns that Mendel observed were true for genes located on different chromosomes, or at least those that were far apart on the same chromosome due to crossing over. Alleles assort independently and we should see predictable even ratios in gametes. But when genes are located close to each other on the same chromosome, they are more often inherited together and are said to be linked. How close are they exactly? This can be determined using data from genetic crosses to calculate recombination frequency. Or, the number of offspring that show a recombination of traits not seen in the parental generation. This segregation probability data can be further applied to calculate relative distance from one gene to another on a chromosome. This is often expressed as map units or centimorgans, named after geneticist Sir Thomas Hunt Morgan. Note that recombination frequency can’t be more than 50%, since this would indicate the alleles are sorting independently.
Lastly, several traits are the product of multiple genes (like skin pigmentation and eye color). These are termed polygenic traits and result in a phenotypic range within a population. Be careful, don’t confuse this with pleiotropic traits, like Marfan Syndrome, which results in one gene affecting multiple characteristics.
Time for unit connections. DNA structure is reviewed in Unit 1 and Unit 6 extends phenotypic expression with the central dogma. Additionally, genetic variation connects to Unit 7: Natural Selection as the driving force of evolution. Alright - what about the exam? Practice those genetics problems! You don’t need to memorize every example (please don’t try), but be familiar with different patterns and learn to recognize them from data sets and pedigrees.
To recap……
Not all inheritance patterns show the predicted ratios of Mendel’s laws. Incomplete dominance, multiple alleles, codominance, sex-linked, recombinants, and polygenetic traits show statistically different phenotypic ratios. Read the problem, identify the parental generation’s gametes, Punnett square and calculate your phenotypic and genotypic ratios. The process is the same, but interpretation differs.
Coming up next on the Apsolute RecAP Biology Edition: Epigenetics
Today’s question of the day is about genetic experiments.
Question of the day: What organism did Sir Thomas Hunt Morgan perform genetic experiments on while developing his chromosomal theory of inheritance?