Class Notes (806,815)
Canada (492,451)
Biology (Sci) (2,417)
BIOL 202 (224)
Lecture 5

BIOL202 Lecture 5 Annotated

37 Pages
Unlock Document

McGill University
Biology (Sci)
BIOL 202
Daniel Schoen

ANNOUNCEMENT(S) Leacock 219 (our satellite room) is closed… LECTURE…. I haven’t quite told you the truth….we have not seen the end of independent assortment quite yet….we do need to cover a few more aspects of it.. Go BACK to lecture 4….last few slides…. Today we will complete the coverage of (simple) multiple gene inheritance….simple in the sense that we are not working with linked genes, or cases where environmental variation can make it difficult to detect the effect of individual genes. And we will also cover briefly a non-nuclear mode of inheritance, cytoplasmic inheritance, which also sometimes is called maternal inheritance….with cytoplasmic inheritance we can also see a sort of independent we do in the case of unlinked nuclear genes,,,,that it assortment of 1 genes carried in the cytoplasm being independent of those in the nucleus……but in this case, the underlying Independent assortment leads to genetic the F2 progeny there are new combinations of traits present…combinations that were not present in the parental generation…..genetic recombination is essentially an outcome of sexual reproduction! In the 1970’s evolutionary biologists began to recognize that the production of males in sexual populations entails a kind of cost. The cost can be understand as follows. On average, a sexual female in a population at carrying capacity will replace herself (otherwise the population must be growing or shrinking). Such replacement means that she will, on average, produce one male and one female offspring, assuming a 1:1 sex ratio. Now consider a rare mutant female that is similar to sexual females in all ways, except that she is asexual. This means that she will reproduce clonally and only produce daughters: two daughters on average (she is asexual). These two daughters will also produce two daughters. Hence, after only two generations, the clone has produced four times as many daughters as the average sexual female. This advantage in daughter production by clones comes as a direct result of the fact that sexual females produce males, which don't make any progeny on their own. Hence, sexual reproduction entails a cost…..there is a cost of producing males. This is not to mean that males contribute nothing to the production of sexual offspring (they contribute genes); it simply means that there is a cost to the sexual population for having 50% on their members not bear their own offspring. So sex and recombination (assortment of traits in new combinations) MUST have SOME advantage. 2 But wait a minute. The vast majority of organisms are sexual. There are only few exceptions. The dandelion and the Bdelloid rotifer are exceptions that reproduce clonally, as in the diagram I just showed. There are no males in the populations of these organisms. So why sex? (next slide) .… what is the advantage that prevents populations from evolving asexuality? 3 I’ll show this advantage (one potential advantage) for a case in which the main form organism is HAPLOID Imagine an environment in which a particular combination of genes, AB, is favored. Maybe these genes produce products that interact in biochemical pathway that is involved in energy production, and those organisms that have both the A and B products, say as enzymes in this pathway can produce the most energy, and in turn, produce the most offspring. Suppose further that the population initially does NOT INITIALLY have any individuals that bear both A and B…….In the clonal population, mutations occur, producing for example, aB or Ab individuals. The population now must “wait” for a second mutation to produce AB. Mutation is a slow process, and so this could take many generations. A sexual population also has mutations. But just like the plant breeder we talked about last time, who crosses individuals and selects desirable combinations of genes, the presence of sex and meiosis quickly produces the AB combination….and the sexual population has an advantage….it may in fact replace the asexual one…..SO INDEPENDENT ASSORTMENT (brought about by meiosis) may be central to life as we know it…..sexual life that is. 4 5 …we had only looked at DUHYBRID crosses….but the same principles apply to more complex ones. Consider this example: a TRIHYBRID CROSS, where the parents are true- breeding (i.e., triple homozygotes for the traits in question) …. (slide) and different for three traits. When these parents are crossed, the resulting F1 progeny are triple heterozygote. They produce many types of gametes (how many?: 2 to the third = 8 types of gametes) that combine in the F2 in 64 ways. We will have to take account of, therefore, a 8 x 8 = 64 cell table. This is cumbersome. With 4 traits, this number rises to 16 x 16 = 256 cell table. Moreover, we may often only want to predict the proportions of a SINGLE type of F2 progeny, and don`t need all the other information available in the table. For example, suppose we wish to predict the proportions of F2 progeny that are tall plants producing, yellow and wrinkled seeds (like parent 1). It is time-consuming to go throughALLof the cells in this 64 cell table. There is a short-cut we can use (as we will see in a moment).... So in this example (of a triple heterozygote), let`s use another method to help us investigate progeny ratios in the F2 generation (next slide).... 6 The short cut is called the lBranching methodz: see text This method works by PARTITIONING a more complex cross into a series of MONOHYBRID crosses…using Mendel’s reasoning about independent assortment, as shown here in the slide. Here is the partitioning: (1) In a MONOHYBRID cross with tall and dwarf, we expect a 3:1 ratio of tall:dwarf progeny in the F2. (2) In MONOHYBRID cross with yellow and green seeded plants, we again expect a 3:1 ratio; this time of yellow:green progeny in the F2. (3)And in a MONOHYBRID cross with round and wrinkled seeded parents, we expect a 3:1 ratio of round:wrinkled progeny in the F2. We can ltie togetherz all these ratios in a ltree-like or branchingz diagram as shown here. So that if were interested in predicting the proportion of the 64 possible outcomes that are TALL, YELLOW, and ROUND, we do this by taking the appropriate PATH through the tree. Likewise, if we wished to predict the proportion of progeny that are TALL, YELLOW, and WRINKLED, we could do this with another path…. (Do it with animation--blue). 7 Both the branching method and the Punnett square become unwieldly. It is better to use the simple product rule from probability theory. This rule states the product of a series of independent events is the product of their individual probabilities. 8 Both the branching method and the Punnett square become unwieldly. It is better to use the simple product rule from probability theory. This rule states the product of a series of independent events is the product of their individual probabilities. 9 Both the branching method and the Punnett square become unwieldly. It is better to use the simple product rule from probability theory. This rule states the product of a series of independent events is the product of their individual probabilities. Total probabiity = 1/2 x 1/2 X 1/2 x 1 x 1/2 x 1/4 = 1/16 x 1/4 = 1/64 10 So we have seen now that SEX (meiosis) produces new combination of genes….and the ability to produce these new combinations may help counteract the cost of sex (cost of males), making it less likely that populations of entirely asexual females would replace populations of sexual females…..again…Mendel’s 2 ndlaw, or what we learn from it, has far-reaching consequences. OK….I alluded to meiosis and the 2 nd law in the same breath…what is the evidence that independent assort is due to chromosomal behaviour in meiosis? It comes from another female scientist…. Estrella Eleanor Carothers (1883-1957), American cytologist and geneticist whose work focused on the cytological basis of heredity. She was especially interested in meiosis….which was by this time was already connected up with Mendel’s 1 law of equal segregation…..She was especially interested in grasshopper chromosomes….. Now why would anyone at this point in the history of genetics select grasshoppers? Why not fruit flies or peas? It turns out that the chromosomes of grasshoppers present a number of advantages to the cytologist. They are large and relatively few in number. The range of chromosome lengths in the complement is such that each chrm pair formed at 11 meiosis can usually be individually identified according to its length. Carothers found a grasshopper in which one chromosome “pair” had nonidentical members….a pair (brown) that nontheless lines up as homologs at meiosis I (remember that HOMOLOGS pair at prophase 1). In the same grasshopper she ALSO found another chromosome (unrelated to the heteromorphic pair) that had no pairing partner at all (purple) at meiosis I She visually screened many meioses and found that there were two distinct patterns (slide— right)….each of these on separate microscope slides, as physical records of what transpired during MEIOSIS 1. In addition, she found that the two patterns were equally frequent! In other words, if we consider each slide in which the pair in brown is constant (), then the unpaired (purple) chromosome was found to go to each pole equally frequently…. half the time with the long form and half the time with the short form. In other words the purple and brown sets were segregating independently. This was considered to be clear proof that chromosomes independently assort during meiosis. 12 So, just so that we are all clear on the implications of Carothers’ work, let’s see how independent assortment of chromosomes leads to (can account for) independent assortment of genes, let’s run through meiosis with two pairs of chromosomes and two pairs of genes, each one located on a separate chrm. Interphase shown here with the homologs not yet replicated or paired up… slide 13 Prophase…chrms have replicated but are not yet paired up 14 The homologs pair up and synapse in prophase….(we’ll come back to this stage in lecture 6, because something interesting happens at this stage…though it is not relevant to today’s topic of independent assortment). BTW, cell biologists have absolutely no idea how the homologs find one another in the nucleus for this synapsis….what attracts them? …. How does the chrm no 1 from your mom, know where to find chrm 1 from you dad, rather than say chrm 2, 3, …. 22? Weird eh? Maybe one of you will work this out. 15 Now, at anaphase 1, we see that there are two equally frequent allelic patterns occur (what Carothers saw essentially), one shown on the lefthand side and the other in on the righthand side. In one manisfestation, the A/A and B/B alleles are pulled together into one cell, and the a/a and b/b are pulled into the other cell. In the other case, the alleles A/A and b/b are united in the same cell and the alleles a/a and B/B also are united in the same cell. The two patterns result from Independent assortment of chromosomes at meiosis. 16 Meiosis then produces four cells from each of these segregation patterns. Because both segregation patterns are equally common, the meiotic product cells of genotypes A; B, a; b, A; b, and a; B are produced in equal frequencies. In other words, the frequency of each of the four genotypes is 1/4. 17 A little aside her
More Less

Related notes for BIOL 202

Log In


Don't have an account?

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.