Did Mendel believe that proteins are hereditary substances?

Did Mendel believe that proteins are hereditary substances?

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Scientists first thought that proteins, which are found in chromosomes along with DNA, would turn out to be the sought-after genetic material. Proteins were known to have diverse amino acid sequences, while DNA was thought to be a boring, repetitive polymer, due in part to an incorrect (but popular) model of its structure and composition.

Was Mendel (1822-1884) one of these scientists?

Note that in 1869, Friedrich Miescher isolated "nuclein," DNA with associated proteins, from cell nuclei. He was the first to identify DNA as a distinct molecule.

The first person to directly indicate a linkage between the hereditary material and enzymes was Garrod in 1902, based on the observation of the hereditary enzymatic disorder alkaptonuria. This is after Mendel's death.

The tetranucleotide hypothesis (i.e. DNA is not informative) that you refer to seems to have been formulated around 1910. So there is no way that Mendel knew about that.

It was not even proposed that proteins were composed of amino acids before 1902. No protein was sequenced before 1950. So Mendel had no idea what sequences or amino acids were, for any biopolymer.

It is formally possible that Mendel knew at some point about Miescher's result, but I'm not aware that he was at all interested in the chemical nature of Mendelian factors (what we now call "genes"). I agree with commenter @jamesqf on this point.

It was not immediately obvious to anyone that there was a discrete mapping between phenotypes and specific agents such as proteins. The major theories of inheritance at the time came from biometricians such as Galton, who believed that inheritance was driven by a blending-like mechanism (more or less), based on phenomena such as regression to the mean. They weren't really interested in the chemical basis either.

Mendelian genetics was only rediscovered around 1900 (Mendel was basically ignored during his lifetime), after which the debate started to consider the question of discrete genetic factors.

In short, I don't think that there is any evidence that Mendel had any interest in chemistry or the chemical relations of the organismal characters he studied.

DNA: as Hereditary Material and Properties of Genetic Material (DNA versus RNA)| Biology

Principles of inheritance given by Mendel and discovery of nuclein (nucleic acids) by Meischer (1871) almost coincided but for claiming that DNA acts as a genetic material took long time. Earlier discoveries made by Mendel, Walter Sutton, T.H. Morgan and others had narrowed the search for genetic material to chromosomes.

Chromosomes are made up of nucleic acids and proteins and are known as hereditary vehicles. In the first instance it appeared that proteins would be hereditary material, until experiments were performed to prove that nucleic acids act as genetic material.

DNA (deoxyribose nucleic acid) has been found to be a genetic material in all the living beings except few plant viruses where RNA is the genetic material because DNA is not found in such viruses.

A. Evidences for DNA as Hereditary Material:

The concept that DNA is the genetic material has been supported by the following evidences:

1. Bacterial Transformation or Transforming Principle (Griffith Effect):

In 1928, Frederick Griffith, a British Medical Officer encountered a phenomenon, now called as bacterial transformation. His observations involved the bacterium Streptococcus pneumoniae (Fig. 6.12) which is associated with certain type of pneumonia. During the course of this experiment, a living organism (bacteria) had changed into living form.

This bacterium is found in two forms:

Whose cells produce a capsule of polysaccharides (mucous), causing the colonies on agar to be smooth and rather shiny? This strain is virulent (pathogenic) and causes pneumonia.

In this case, cells lack capsule and produce dull rough (R) colonies.

Presence or absence of capsule is known to be genetically determined.

Both S and R strains are found in several types and are known as S-I, S-II, S-III etc. and R-I, R-II and R-III etc. respectively.

Mutations from smooth to rough occur spontaneously with a frequency of about one cell in 10 7 though, the reverse is much less frequent.

Griffith performed his experiment by injecting the above bacteria into mice and found the following results:

(a) S-III (virulent) bacteria were injected into mice the mice developed pneumonia and finally died.

(b) R-II (non-virulent) bacteria were injected into mice the mice suffered no illness because R-II strain was non-pathogenic.

(c) When Griffith injected heat killed S-III bacteria into mice, they did not suffer from pneumonia and thus survived.

(d) A mixture of R-II (non-virulent) and heat killed S-III bacteria were injected into mice the mice developed pneumonia and died. By postmortoming the dead mice, it was noticed that their heart blood had both R-II and S-III strains of bacteria.

Thus some genetic factor from dead S-III cells converted the live R-II cells into live S-III cells and the latter produced the disease. In short, living R-II cells were somehow transformed. So the Griffith effect gradually became known as transformation and turned out to be the first step in the identification of genetic material.

Biochemical Characterization of Transforming Principle:

Identification of Transforming Genetic Substance:

In 1944, sixteen years after Griffith’s experiment, Oswald Avery, Colin MacLeod and Maclyn McCarty (1933-1944) reported successfully repetition of bacterial transformation, but in vitro. They were able to identify the transforming genetic material. They tested fractions of heat killed cells for transforming ability. Their findings were as under.

(i) DNA alone from S bacteria caused R bacteria to become transformed.

(ii) They found that proteases (protein digesting enzymes) and RNAse (RNA digesting enzymes) did not affect transformation.

(iii) Digestion with DNAase did inhibit transformation.

Thus they finally concluded that DNA is the hereditary material.

Mixture injected into healthy mice

1. R-U type living cells + Capsule of heat killed S-III type.

Mice did not develop pneumonia.

2. R-II type living cells + Cell wall of heat killed S-III type.

3. R-II type living cells + Cytoplasm of heat killed S-III type (without DNA)

4. R-II type living cells + DNA of heat killed S-III type.

Mice developed pneumonia and died.

5. R-II type living cells + DNA of heat killed S-III type + DNAase

Mice did not develop pneumonia.

Therefore, it is now beyond any reasonable doubt that DNA is the hereditary material.

2. Bacteriophage Infection:

Viral infecting agent is DNA. By using radioactive tracers, Alferd Hershey and Maratha Chase (1952) gave evidence that DNA is the hereditary material in certain bacteriophages (bacterial viruses).

Structure of T2 bacteriophage:

This bacterial virus contains an outer non-genetic protein shell and inner core of genetic material (DNA). The T2 phages are of tadpole shape differentiated into head and tail region. Head is an elongated, bipyramidal, six sided structure composed of several proteins.

Within the head (Fig. 6.13) is a closed, non-ending DNA molecule. The dimensions of head is such that it is able to pack DNA molecule tightly inside it. The tail is a hollow cylinder. The tail bears 24 helical striations.

(ii) Some other bacteriophages were grown in bacteria having 32P. This radioactive 32P was restricted to DNA of phage particles.

Six tail fibres appear from an hexagonal plate at the distal end of plate. Tail is formed of proteins only. Proteinaceous outer shell contains sulphur (S) but no phosphorus (P), whereas DNA contains phosphorus but no sulphur.

Hershey and Chase (1952) conducted their experiment on T2 phage which attacks the bacterium Escherichia coli.

The phage particles were prepared by using radio isotopes of 35 S and 32 P in the following steps:

(i) Few bacteriophages were grown in bacteria containing 35 S.This radioactive was 35 S incorporated into the cysteine and methionine amino acids of proteins and thus these amino acids with 35 S formed the proteins of phage.

(ii) Some other bacteriophages were grown in bacteria having 32 P. This radioactive 32 P was restricted to DNA of phage particles.

These two radioactive phage preparations (one with radioactive proteins and another with radioactive DNA) were allowed to infect the culture of E. coli. The protein coats were separated from the bacterial cell walls by shaking and centrifugation.

The heavier infected bacterial cells during centrifugation pelleted to bottom (Fig. 6.14). The supernatant had the lighter phage particles and other components that failed to infect bacteria.

It was observed that bacteriophages with radioactive DNA gave rise to radioactive pellets with 32 P in DNA. However in the phage particles with radioactive protein (with 35 S) the bacterial pellets have almost nil radioactivities indicating that proteins have failed to migrate into bacterial cell.

So, it can be safely concluded that during infection by bacteriophage T2, it was DNA which entered the bacteria. It was followed by an eclipse period during which phage DNA replicates numerous times within the bacterial cell (Fig. 6.15).

Towards the end of eclipse period phage DNA directs the production of protein coats assembly of newly formed phage particles. Lysozyme (an enzyme) brings about the lysis of host cell and releases the newly formed bacteriophages.

The above experiment clearly suggests that it is phage DNA and not protein which contains the genetic information for the production of new bacteriophages. However, in some plant viruses (like TMV), RNA acts as hereditary material (being DNA absent).

B. Properties of Genetic Material (DNA versus RNA):

DNA is the genetic material RNA has been found to be genetic material in TMV (Tobacco mosaic virus), ф β bacteriophage etc. DNA is major hereditary material in most of the organisms. RNA mainly performs the functions of messenger and adapter. This is mainly due to differences between chemical structure of DNA and RNA.

Required properties of genetic material:

This refers to duplication of its genetic material by faithful replication which is shown by both DNA and RNA. Proteins and other molecules present in living being do not exhibit this property.

Stability of genetic material should exist. It should not change its structure easily with changed stages of life, age of physiology of living beings. Even in Griffith’s experiment of ‘transforming principle’, DNA survived in heat killed bacteria. Both the strands of DNA which are complementary can be separated.

RNA is liable and easily degradable due to presence of 2’—OH group present in each nucleotide. As RNA is catalytic, it has become reactive. Because DNA is more stable than RNA, it is said to be better genetic material. Presence of thymine instead of uracil is another reason which leads to stability of DNA.

Genetic material should be able to undergo mutation and such a change should be stably inherited. Both nucleic acids DNA and RNA have the capacity to mutate. RNA mutates at a faster rate when compared with DNA. Virus with RNA genome show mutation and evolution at a faster rate and thus has shorter life span.

Table 6.6. Types of nucleic acids:

Macromolecule in shape of double helix with many thousands of sub- units.

Mainly in nucleus, also in mitochondria and chloroplasts.

Acts as store of coded instruc­tions for synthesis of all proteins required by the cell.

Messenger ribonucleic acid.

Single-stranded polymer with hundreds of sub-units.

In nucleus and cytoplasm especially ribosomes.

Made on the DNA template it carries coded instructions for synthesis of one or more proteins from nucleus to ribosomes.

Ribosomal ribonucleic acid.

Molecule very closely bound to protein fraction.

Forms part of ribosome structure. Helps in locating mRNA correctly on ribosome surface.

Transfer ribonucleic acid.

Single-stranded polymer of less than one hundred sub- units.

Many kinds of tRNA act as amino acid carriers. Take specific amino acid from cytoplasm to mRNA tem­plate on ribosome.

4. Genetic expression:

RNA expresses easily the characters in the form of proteins. DNA requires RNA for formation of proteins. DNA being more stable is considered better than RNA for storage of genetic information. However, for transmission of genetic characters, RNA gives better results.

DNA, the Genetic Material

DNA, deoxyribonucleic acid, is the genetic material in your cells. It was passed on to you from your parents and determines your characteristics. The discovery that DNA is the genetic material was another important milestone in molecular biology.

Griffith Searches for the Genetic Material

Many scientists contributed to the identification of DNA as the genetic material. In the 1920s, Frederick Griffith made an important discovery. He was studying two different strains of a bacterium, called R (rough) strain and S (smooth) strain. He injected the two strains into mice. The S strain killed (virulent) the mice, but the R strain did not (non-virulent) (see Figure below). Griffith also injected mice with S-strain bacteria that had been killed by heat. As expected, the killed bacteria did not harm the mice. However, when the dead S-strain bacteria were mixed with live R-strain bacteria and injected, the mice died.

Griffith&rsquos Experimental Results. Griffith showed that a substance could be transferred to harmless bacteria and make them deadly.

Based on his observations, Griffith deduced that something in the killed S strain was transferred to the previously harmless R strain, making the R strain deadly. He called this process transformation, as something was "transforming" the bacteria from one strain into another strain. What was that something? What type of substance could change the characteristics of the organism that received it?

Avery&rsquos Team Makes a Major Contribution

In the early 1940s, a team of scientists led by Oswald Avery tried to answer the question raised by Griffith&rsquos results. They inactivated various substances in the S-strain bacteria. They then killed the S-strain bacteria and mixed the remains with live R-strain bacteria. (Keep in mind, the R-strain bacteria usually did not harm the mice.) When they inactivated proteins, the R-strain was deadly to the injected mice. This ruled out proteins as the genetic material. Why? Even without the S-strain proteins, the R strain was changed, or transformed, into the deadly strain. However, when the researchers inactivated DNA in the S strain, the R strain remained harmless. This led to the conclusion that DNA is the substance that controls the characteristics of organisms. In other words, DNA is the genetic material. You can watch an animation about the research of both Griffith and Avery at this link:

Hershey and Chase Seal the Deal

The conclusion that DNA is the genetic material was not widely accepted at first. It had to be confirmed by other research. In the 1950s, Alfred Hershey and Martha Chase did experiments with viruses and bacteria. Viruses are not made of cells. They are basically DNA inside a protein coat. To reproduce, a virus must insert its own genetic material into a cell (such as a bacterium). Then it uses the cell&rsquos machinery to make more viruses. The researchers used different radioactive elements to label the DNA and proteins in viruses. This allowed them to identify which molecule the viruses inserted into bacteria. DNA was the molecule they identified. This confirmed that DNA is the genetic material.

Mendel's experiment

Figure 2: The fruit-bearing pod of Pisum satvium, the common pea plant used by Gregor Mendel in his breeding experiments.

Gregor Johann Mendel was an Austrian monk who performed experiments in a monastery known for its scientific as well as its religious pursuits. Beginning in 1843, Mendel undertook experiments to understand the particulars of heredity, initially breeding normal and albino mice and then looking at the coat color of the offspring. Mendel's experiments with mice proved unsatisfactory since the mice took too long to breed and bore so few young in each litter. Additionally, they smelled terrible and some people felt animal breeding experiments were carnal and inappropriate work for a monk. Consequently, Mendel began looking at inheritance in plants, using Pisum stavium, the formal name for simple garden peas (Figure 2). Many varieties of this plant existed, peas were inexpensive and could be grown in rows of pots in the monastery garden, and each plant gave Mendel many peas to examine.

Figure 3: Pea flowers.

Breeding plants was different from breeding mice, but Mendel still had matchmaking work to perform. Flowering plants (Figure 3) have both male and female reproductive parts. The pollen of a flower, found on the flower's anthers, is similar to sperm cells in other organisms and the flower's egg cells, called ovules, are kept separate from the pollen by hiding them inside a compartment called the carpel. Breezes or bugs can transfer pollen from the anthers of one flower and leave it on the carpel of another ("cross-pollination"). Just as easily, pollen can travel from the anthers to the carpel of the same flower, resulting in self-pollination. Using a paintbrush, Mendel played the part of a selective insect and pollinated particular plants by brushing the powder from the anthers of one variety onto the carpel of another. To avoid any self-pollination, Mendel also "emasculated" the recipient plants, using tweezers to snip off their anthers. Some might have thought that this, too, was odd work for a monk, but Mendel persisted.

Figure 4: Two of the different phenotypes expressed by Pisum satvium.

Mendel chose seven physical traits (now referred to as phenotypes) to study: flower color and placement, pod color and shape, pea color and shape, and plant size (Figure 4). These were all easily observable properties of the plants and so could be quickly counted. Mendel's goal was to reveal the genetic makeup (now called genotype) underlying each variety of pea plant and to understand how each trait was inherited. Performing his experiments took at least as much patience as skill. Mendel began by making "pure breeding" plants, ones that reliably gave rise to plants of the same physical traits generation after generation. This alone took him two years but gave him confidence in the genetic makeup of his starting plants, which he called the parental generation of his experiment.

Using his paintbrush, Mendel's next step was to cross-pollinate parental plants with different physical traits, yielding offspring that were the hybrid of two different plants. He recorded the appearance of each trait in the hybrid offspring plants, called the first filial generation (or F1 generation), and then followed the inheritance pattern to the next generation by self-pollinating the F1 plants to produce the second filial generation (F2) and carefully recording each variety that arose. Mendel's mathematical approach to the question of inheritance is one of his greatest legacies. In genetics (as in other sciences) it is easy to be misled by the results of a few experiments. Flip two coins and they may both show heads, but flip 1,000 coins and the split of heads to tails will be nearly even. In Mendel's case he examined more than 1,000 plants for their size and more than 8,000 peas for their color.

The observable physical traits of an organism are called

A New Model of Inheritance

Illustration of the common type of pea plants (Pisum sativum) Mendel used in his experiments. Wikimedia: Prof. Dr. Otto Wilhelm Thomé Flora von Deutschland, Österreich und der Schweiz

Mendel’s experiments with peas were able to disprove blended inheritance and show that genes are actually discreet units that keep their separate identities when passed from generation to generation. One of the reasons for the success of Mendel’s experiments was that they were very carefully designed and controlled. This was possible due to his strong understanding of the natural world and the life cycle of plants. Mendel also kept detailed notes of everything that he did and what he observed. In addition, Mendel was familiar with both mathematics and probability. This knowledge is what allowed him to see patterns in the outcome of his experiments and realize what those patterns meant.

The entire set of pea experiments took eight years to complete (1856-1863). In 1865, Mendel published his findings in a paper called Experiments on Plant Hybridization, which was mostly ignored at the time due to a number of reasons. First, Mendel was not well known in the scientific community. Second, his theory ran against the popular model of blended inheritance. His work also used mathematics and probability, which was a very unusual way to approach a scientific problem at the time and difficult for many people to understand.

It was more than thirty years after Mendel’s paper was published until the importance of his work was truly appreciated. Mendel's experiments are a good example that scientific discoveries are sometimes slow to be added to the collection of scientific knowledge. It took time for the community to fully understand his work and the methods he used to unlock one of the early mysteries of genetics. It is also interesting to know that while Mendel was a great thinker and scientist, he also failed two of his major exams needed to become a teacher. Many believe he had terrible test anxiety when taking exams. You could be someone that has similar problems when facing a big test. Just knowing that there have been and still are people that have the same problem might be helpful when you take your next exam.

Klug, W.S., Cummings, M.R., Spencer, C. (2005) Concepts of Genetics, 8th Edition. Menlo Park, CA: Benjamin Cummings

Heller, H.C., Orians, G.H., Purves, W.K., Sadava, D. (2003) Life: The Science of Biology, 7th Edition. Sunderland, MA: Sinauer Associates, Inc. & W. H. Freeman and Company

Henig, R. M. (2001) The Lost and Found Genius of Gregor Mendel, the Father of Genetics. New York, NY: Houghton Mifflin. Retrieved from

* Courtesy of American Philosophical Society, Curt Stern Papers - Cold Spring Harbor Laboratory.

Additional images and illustrations from Wikimedia Commons. Pea photo by Rasbak.

Will Taupo erupt soon?

Because volcanic activity can signal imminent eruptions, the researchers noted that New Zealand officials probably should have issued an alert for "minor volcanic unrest." However, they acknowledged that it would have been difficult for officials to determine the cause of the earthquakes in real time. After all, it's not easy to monitor volcanoes, especially Taupo, much of which lies under a 238-square-mile lake. It's even harder to forecast eruptions. One key reason is that volcanic unrest always precedes eruptions, but eruptions don't always follow volcanic activity.

Satellite view of the Taupo volcanoCredit: NASA / NASA World Wind

Since the Ōruanui eruption, the Taupo volcano has erupted at least 28 times, the most powerful of which was the eruption that occurred around the year 232. What are the chances of Taupo erupting with similar force in our lifetimes? Not great. A 2020 paper published in Earth and Planetary Science Letters put the annual odds of such an eruption occurring over the next 500 years between 0.5 and 1.3 percent. Magma needs more time to accumulate before a super-eruption is likely.

Still, volcanic eruptions worldwide have killed about 2,000 people since 2000, 22 of whom died when a stratovolcano on New Zealand's White Island erupted in 2019. The researchers behind the new study said their findings highlight the need for improved monitoring techniques.

"Our findings show that Taupo needs to be carefully monitored to better understand the processes at depth and the factors that might cause similar unrest to escalate into an eruption in the future," the researchers wrote.

Course Organization

The General Genetics class was offered each year as two separate but parallel sections with about 30 students each and met for 50 minutes three times a week. Each class was based on a PowerPoint presentation, but often included examples of relevant data or sample problems. Creighton uses an in-class video recording system so all the PowerPoint presentations and the class audio were digitally saved for later review. A written handout was provided for each class with a summary of the lecture material, a list of specific terms to define and know, and problems from the textbook to be answered. There were no graduate assistants or separate recitation sections, but undergraduate assistants offered tutoring sessions, and I held extensive office hours/problem sessions each week. The initial enrollments were similar over the two years. In the Fall semester of 2014, there were a total of 52 students, which included no sophomores, 27 juniors, and 25 seniors. In the Fall semester of 2015, the initial enrollment was again 52 students, but included 12 sophomores, 18 juniors, and 22 seniors. This reflected a difference in the advising process in which some Biology majors were encouraged to take the class sooner. The sequences of topics for the two versions of the course are shown in Table 1.

Fall 2014—“Mendel first” . Fall 2015—“molecules first” .
The genetic system The genetic system and genetic analysis
Inheritance of single genes in eukaryotes DNA structure and organization into chromosomes
Variations in single gene inheritance DNA replication and transmission in prokaryotes
Inheritance of independently assorting genes DNA replication and transmission in eukaryotes
Inheritance of organelle genes Transcription in prokaryotes
Gene interactions Transcription and RNA processing in eukaryotes
Inheritance of linked genes and recombination Protein synthesis
Mapping genes on eukaryotic chromosomes Cloning and sequencing of DNA
Mapping genes in bacteria Transcriptomes and proteomes
DNA structure and chromosome organization Inheritance of single genes in eukaryotes
DNA replication Sex linkage and human pedigree analysis
Transcription Dihybrid crosses and independent assortment
RNA processing Variations in Mendelian patterns
Protein synthesis Polygenic traits and epistatic interactions
Regulation of gene expression in bacteria Organelle genetics
Regulation of gene expression in eukaryotes Inheritance of linked genes and recombination
Transposable elements Mapping genes on eukaryotic chromosomes
Mutation Mapping genes in bacteria
DNA Repair Molecular mechanisms of recombination
Recombination and recombinational repair Regulation of gene expression in bacteria
Large-scale chromosomal changes Regulation of gene expression in eukaryotes
Population genetics Transposable elements
Inheritance of complex traits Large-scale chromosomal changes
Fall 2014—“Mendel first” . Fall 2015—“molecules first” .
The genetic system The genetic system and genetic analysis
Inheritance of single genes in eukaryotes DNA structure and organization into chromosomes
Variations in single gene inheritance DNA replication and transmission in prokaryotes
Inheritance of independently assorting genes DNA replication and transmission in eukaryotes
Inheritance of organelle genes Transcription in prokaryotes
Gene interactions Transcription and RNA processing in eukaryotes
Inheritance of linked genes and recombination Protein synthesis
Mapping genes on eukaryotic chromosomes Cloning and sequencing of DNA
Mapping genes in bacteria Transcriptomes and proteomes
DNA structure and chromosome organization Inheritance of single genes in eukaryotes
DNA replication Sex linkage and human pedigree analysis
Transcription Dihybrid crosses and independent assortment
RNA processing Variations in Mendelian patterns
Protein synthesis Polygenic traits and epistatic interactions
Regulation of gene expression in bacteria Organelle genetics
Regulation of gene expression in eukaryotes Inheritance of linked genes and recombination
Transposable elements Mapping genes on eukaryotic chromosomes
Mutation Mapping genes in bacteria
DNA Repair Molecular mechanisms of recombination
Recombination and recombinational repair Regulation of gene expression in bacteria
Large-scale chromosomal changes Regulation of gene expression in eukaryotes
Population genetics Transposable elements
Inheritance of complex traits Large-scale chromosomal changes

Some topics were covered in a single class period, but others took a period and half or two periods. The schedule was adjusted during the semester, and some topics that were initially included, such as Developmental Genetics, were dropped as I learned more about the department's curriculum.

The courses were similar in that each had four or five in-class exams consisting of two parts. Part I was a set of 30 multiple-choice questions worth 2 points each for a total of 60 points. These questions were a combination of relatively simple genetic problems and those that tested student comprehension of the basic genetic facts or concepts. Part II consisted of four genetic problems or short-answer questions worth 10 points each for a total of 40 points. The genetic problems were more complex than those in the multiple-choice section and often involved multistep calculations. The short-answer questions were usually introduced with a figure similar to one used in the textbook or in the PowerPoint presentations given in class and involved several subparts. In addition to the exams, there were eight to ten homework assignments each year that could be completed individually or in small groups. Again, depending on the material, the homework assignments consisted of genetic problems of different types or short-answer questions. I also had the students in the Fall 2014 class write a term paper on a topic of their own choosing about genetics, but I dropped this assignment for the Fall 2015 class.

There were several reasons for changing the approach from “Mendel first” to “molecules first” in the second year. First, I found that students who had Cell Structure and Function before taking General Genetics appeared to do better on each of the five exams in 2014 (Figure 1). Exams 1 and 2 focused on Mendelian genetics, Exams 3 and 4 focused on molecular genetics, and Exam 5 covered a mixture of topics. Although the standard deviations were relatively large, an ANOVA analysis of the data (Vasavada, 2016) indicated significant differences among all 10 of the exam scores (F-statistic = 6.23, p-value = 8.34 × 10 -8 ). A Tukey HSD (honestly significant difference) post-test analysis as well as Scheffé and Bonferroni and Holm comparisons indicated the most consistent significant differences were between the scores on Exam 4 and the scores on Exam 5. However, on any individual test, there were no significant differences between those students who had taken Cell Structure and Function and those who had not.

Mean percentage scores on the five exams in General Genetics (±1 SD) for the Fall semester of 2014. The open bars show the scores for students who had not taken Cell Structure and Function prior to enrolling in Genetics. The filled bars show the scores for students who had taken Cell Structure and Function prior to enrolling in Genetics. An ANOVA analysis of the data was done with an online program (Vasavada, 2016), and post-test analysis indicated that the only significant differences were between the scores on Exam 4 and Exam 5 for each group.

Mean percentage scores on the five exams in General Genetics (±1 SD) for the Fall semester of 2014. The open bars show the scores for students who had not taken Cell Structure and Function prior to enrolling in Genetics. The filled bars show the scores for students who had taken Cell Structure and Function prior to enrolling in Genetics. An ANOVA analysis of the data was done with an online program (Vasavada, 2016), and post-test analysis indicated that the only significant differences were between the scores on Exam 4 and Exam 5 for each group.

Second, I thought that some Mendelian concepts like dominance, epistasis, and variable penetrance would make more sense if students understood how genes worked and contributed to a phenotype. If a student does not know that genes direct the synthesis of proteins, and that gene products interact to produce observable phenotypes, these concepts are often obscure. In a similar way, genetic exchange and gene mapping in bacteria are better understood if a student knows how DNA replication and molecular recombination work. Third, I felt that because the material in molecular genetics is somewhat more descriptive, students might do better on the exams at the beginning of the course. They would thus develop enough confidence to cope better with the more difficult analytical material that is involved in the interpretation of crosses in Mendelian genetics.

Avery-Macleod-McCarty experiment

In 1944, Oswald Avery, Colin MacLeod and Maclyn McCarty helped demonstrate the role of DNA as the carrier of genetic information by working with the bacterium that causes pneumonia, Streptococcus pneumoniae.

Frederick Griffith identified the ‘transforming principle’.

However, their work was given a head start by a British bacteriologist called Frederick Griffith, who identified something called the ‘transforming principle’.

Frederick studied two strains of the Streptococcus pneumoniae bacteria. One, called the S strain, had smooth walls and was fatal when injected into mice. The second strain, R, had rough walls and was not fatal when injected into mice. The S strain was smooth due to a coat made out of sugars that helped protect it from the mouse immune system. The rough R bacteria were rough because it did not have a sugar coat, and so was not protected from the mouse immune system.

Frederick carried out a series of experiments to investigate the strains further.

  1. First he killed S bacteria with heat and injected them into the mice. The mice survived.
  2. He then injected heat-killed S bacteria along with living R bacteria. The mice died.
  3. After studying the blood of these mice he was surprised to find living S bacteria in it, somehow the rough R bacteria had transformed into smooth S bacteria.
  4. He then came to the conclusion that there was a ‘transforming principle’ responsible for this.

But what exactly was it? Was it the proteins in the bacteria, the sugar coat on the S bacteria, the immune system of the mouse or the nucleic acids RNA and DNA?

Enter Oswald Avery and his colleagues. Working in test tubes, they used detergent to break open the heat-killed S cells to separate out the different components:

They then destroyed the components one by one to identify which component was the ‘transforming principle’. The team published their results in 1944.

  1. First they combined the heat-killed S bacteria with an enzyme that broke down the smooth sugar coat. They then mixed the sugar-coatless S bacteria with the R bacteria and found that the R bacteria still transformed into S bacteria. So, the ‘transforming principle’ was not in the sugar coat.
  2. Next they added protein-digesting enzymes to destroy all of the protein in the bacteria, and yet again when mixed with R bacteria, the R transformed into S. So the ‘transforming principle’ clearly wasn’t a protein either.
  3. Next they isolated the nucleic acids, DNA and RNA, using alcohol.They then destroyed the RNA using the RNase enzyme, leaving just the DNA behind. They mixed it with the R bacteria, and transformation from R to S still occurred. So, it wasn’t RNA.
  4. Finally, they destroyed the DNA in the solution using DNase, mixed it with the R bacteria, and no transformation occurred, the R bacteria remained rough. So, the ‘transforming principle’ must be DNA!

Image credit: Genome Research Limited

From Aristotle to Weismann

Before the nineteenth century, questions about offspring looking like their parents were asked within a conceptual framework that embraced very different assumptions than scientists do today. The contributions of the parents to the offspring were not necessarily assumed to be equal, or even to be purely material. The ancient Greek philosopher Aristotle, for example, thought that the male semen contributed the ⊬tive element" to the offspring, bringing it to life, while the female contributed only nutritional material for the offspring.

Theorists who did think both parents contributed some material elements generally assumed that blending inheritance held true: the parental contributions were believed to blend together so that the offspring's characteristics were usually intermediate between those of the parents. If one parent had a short nose and another a long one, the child could be expected to have a nose somewhere in between. Moreover, in this conceptual framework, heredity was not separated sharply from environment it was Ȭommon sense" that environmental effects on parental characteristics could reappear in their offspring. (This would later be called "the inheritance of acquired characters," or "Lamarckism," after the early-nineteenth-century biologist Jean-Baptiste Lamarck.) Thus, if parents were well educated, it was assumed that their children would be smart.

In the late nineteenth century, this framework was gradually abandoned. Two shifts in outlook were especially important. First, spurred on by new observations, scientists came to view hereditary transmission as a purely material process (possibly exempt from the effects of the environment). Starting in the 1860s, biologists developed new microscopic techniques to study the physical processes of the cell (a branch of biology called cytology ). In 1875, the German anatomist Oscar Hertwig was the first to observe a sperm penetrating an egg (of a sea urchin), thereby lending credence to the idea that a material substance was actually physically transferred via the sperm.

In the 1870s, new structures in the nucleus were discovered, called chromosomes (which means Ȭolored bodies") because they absorbed dyes more intensely than the surrounding nuclear material. Although their function was mysterious, the fact that they came in pairs (perhaps one from each parent) suggested a possible role in heredity. As cytologists raced to sort out the complex and confusing cell-division events of mitosis and meiosis from the late 1870s to the early 1900s, they constructed innovative theories of heredity to accommodate these new observations. In contrast with earlier work, most of these theories postulated that some physical substance carried by the sperm and egg combined during fertilization to produce the offspring.

August Weissmann. At the same time, theorists began to challenge a second fundamental assumption of the old framework: blending inheritance. Instead, they suggested that inheritance was particulate: each parent contributed to the offspring its own share of discrete units corresponding to some hereditary trait (such as height or eye color), which were somehow then combined and sorted in the offspring. In the 1880s and 1890s, the German zoologist August Weismann influentially combined the two new concepts (material transfer and particulate inheritance), postulating a substance called the "germ plasm" that was carried in the chromosomes of the reproductive cells from generation to generation, and that was made up of invisible particles corresponding to particular body structures. Though Weismann's theory was highly speculative, by the early 1900s studies of chromosomal action during fertilization and early development seemed to confirm important parts of it, especially the role of the chromosomes as bearers of particulate hereditary material.

Weismann was not the only theorist to propose that the hereditary material was made up of discrete particles: Charles Darwin had conceived of heredity as particulate in the late 1860s (though his theory of heredity was not well regarded), and the Dutch plant breeder Hugo de Vries theorized a hereditary particle he called the "pangene." Thus, in 1900 scientists were already thinking about hereditary particles when de Vries and the German botanist Carl Correns rediscovered an obscure paper published in 1865 by the Austrian monk Gregor Mendel.

Gregor Mendel. Describing his breeding experiments on the common garden pea, Mendel developed his basic concept of paired, discrete hereditary 𢾬tors" (he did not call them "genes" or Ȫlleles"). Each parent contributed one factor for each trait, and each trait came in one of two forms, dominant or recessive. Although only the dominant form would be visible in any combination of dominant and recessive, the recessive factor was still there, hidden, and could be passed to the next generation. If two recessives combined together, then the recessive form would be Ȯxpressed." Mendel's results also supported the idea that traits such as height and seed texture were not generally linked but recombined randomly during reproduction, showing independent assortment. A tall pea plant could thus have either smooth or wrinkled seeds so could a short pea plant. In 1909, the Danish Mendelian Wilhelm Johannsen named these presumed hereditary particles "genes."

Mendel's ideas commanded immediate, widespread interest. His peabreeding experiments, which ran over many generations of plants to yield impressively stable statistical ratios of hereditary traits, provided biological theorists with compelling new evidence for the hypothesis of paired hereditary characters that sorted independently. Mendel's results appeared to offer practical guidance as well. Animal and plant breeders believed that they would help them develop rational systems for combining desirable traits in livestock and agriculturally important plants. Eugenicists, who sought to improve the human race through breeding "the best" traits together (such as strength and intelligence), thought Mendelism would provide rules for rational human breeding.

Thomas Hunt Morgan. By the early 1900s, then, the existence of discrete genes that governed heredity seemed plausible to most biologists. However, the location and the physical nature of these theoretical entities was still uncertain. In particular, the relation between genes (which seemed to come in pairs) and chromosomes (which also came in pairs) was still a matter of some debate. Then in the 1910s, Thomas Hunt Morgan at Columbia University united the cytological focus on chromosome activity with the Mendelian breeding approach.

Combining breeding experiments on fruit flies ( Drosophilia ) with microscopic study of their chromosomes, Morgan and his students established beyond any doubt that hereditary material was carried on the chromosomes and that the theoretical entity known as the gene corresponded to particular identifiable traits. They also refined the theory of the gene substantially, developing explanations for "linked" traits that did not sort randomly (genes near each other on the same chromosome), positing the existence of more than two forms of a gene (multiple alleles ), and developing the idea that some genes could act as modifiers on others, changing their effect.

Morgan's student Alfred H. Sturtevant combined breeding experiments, statistical analysis, and the study of chromosomes under the microscope to draw up chromosome "maps" that showed how far apart the genes for various traits must be on the chromosome. Although some scientists outside Morgan's powerful circle𠅎specially in Europe𠅌ontested the view that the chromosomal gene was the sole bearer of hereditary material (arguing, for example, that the cytoplasm surrounding the nucleus might also play a role in heredity), the views established by Morgan and his school in the 1910s and 1920s largely prevailed, and have come to be known as classical genetics.

Biochemistry. Biologists in the Morgan tradition, however, were unequipped to answer the question, What is the gene made of? Answering this question required attention to biochemistry. In the 1930s and 1940s, the leading candidate was protein , though a minority view held that it might be deoxyribonucleic acid, or DNA. In 1944, Oswald Avery, Colin MacLeod, and Maclyn McCarty published results of their experiments with the pneumonia-causing bacterium Streptococcus pneumoniae that indicated that DNA was the right pick, and in 1952 this view gained strong verification by the famous "Waring blender" experiments of Alfred Hershey and Martha Chase, which showed that the protein of the bacteriophage virus was a mere protective coating, while the stuff that created genetic transformation was DNA.

In 1953, James Watson and Francis Crick went further, postulating a double-helical structure for DNA, arguing that the four nucleotide bases guanine, cytosine, thymine, and adenine were its building blocks. The parallel structure of the helices suggested the possibility that it "unzipped" in replication, such that each side of the zipper, each helix, could then act as a template for the synthesis of a complementary strand of DNA, thus creating a perfect replica, ideally suited for passing on to offspring. Finally, in the early 1960s, scientists interpreted the sequence of nucleotides along the chromosome as a code for the sequence of amino acids in protein. This insight illuminated the means by which the gene dictates the physical characteristics of the organism possessing it. Although many details needed to be resolved, it seemed to many that the most basic keys to heredity had been discovered.

By the late twentieth century, then, biologists had come to view the gene from two directions. Working from the "outside in," organismal and population biologists continued to operate with the classical concept that a gene (or some combination of genes) corresponds to a trait (as in Ȫ gene for X"). Working from the "inside out," biochemists and molecular biologists defined the gene as the amount of DNA that codes for one protein or one polypeptide . Since a protein is not the same as a trait, much work continues to aim at unravelling the complex nature of gene expression . As research continues to develop, and the field of genomics continues to expand, the idea of the gene continues to evolve.

Science: Molecular biology solves the riddle of Mendel's wrinkly peas

WHEN in the 1860s, Gregor Mendel made his seminal studies of heredity
in pea plants, he knew nothing about the molecular basis for his rules.
Now, a team of researchers in Britain has cloned the gene responsible for
one of the characteristics that Mendel described in the pea seeds: wrinkles.

Mendel observed seven pairs of characteristics in peas. They include
tallness and dwarfishness, colour or colourlessness in the flower, and differences
in the shape and colour of the seed. He found that the peas were either
round or wrinkled, and that the round character was dominant to the wrinkled
character. The factors that governed these two phenotypes were later labelled
as R and r respectively.

Since then, other researchers have shown that there is a marked difference
between the starch in the round (RR or Rr) peas and the wrinkled (rr) ones.
In 1988, Alison Smith at the John Innes Institute in Norwich found that
the structure of the starch depended on the presence or absence of one of
two forms of an enzyme called the starch-branching enzyme I (SBEI).

A seed that lacks the enzyme has a higher sugar content than one that
has the enzyme. This makes it accumulate more water than its counterpart,
so it swells to a larger size at an early stage in its development, and
shrinks as it dries out. The shrinkage gives it its wrinkled appearance.
Smith found that the rr peas always lacked SBEI.


Now Madan Bhattacharyya, Cathie Martin and their colleagues at the institute
have cloned the fragment of DNA that encodes SBEI from the pea that Mendel
would have used, Pisum sativum, and demonstrated that it lies at the r locus
(Cell, vol 60, p 115).

They found that the messenger RNA transcript of the SBEI gene in rr
seeds was much bigger than in RR forms. And rr seeds produced only about
one-tenth of the amount of transcript that RR seeds did, weight for weight.

Finally, the team found that the extra genetic material in the sequence
coding for SBEI was an inserted fragment, about 800 base pairs long and
with repeated base pairs at either end. According to the researchers, this
fragment is very similar to certain transposable sequences of DNA in other
plants such as maize. The insertion causes the wrinkled phenotype, rr, because
it prevents the normal expression of the SBEI gene.

Bhattacharyya and his colleagues conclude that ‘since all the data Mendel
provided fit the assumption that he used the r mutant and since there is
no other evidence of another mutation available at this time, we believe
that the gene we have cloned is the one studied by Mendel’.

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