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Jacob, monod, the lac operon, and the pajama experiment—gene expression circuitry changing the face of cancer research.

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• Version of Record April 14 2016

Stephen B. Baylin; Jacob, Monod, the Lac Operon, and the PaJaMa Experiment—Gene Expression Circuitry Changing the Face of Cancer Research. Cancer Res 15 April 2016; 76 (8): 2060–2062. https://doi.org/10.1158/0008-5472.CAN-16-0865

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Visit the Cancer Research 75 th Anniversary timeline .

See related article by Pitot and Heidelberger, Cancer Res 1963;23:1694–700 .

It is a virtually universal rule in science that if we step back to reflect upon a field currently viewed as extremely dynamic and novel, we find ourselves standing on the shoulders of those whose seminal observations gave birth to it far earlier. For those of us working in the fields of signal transduction and epigenetics within the cancer research arena, this is absolutely the case when we consider the brilliant realizations of Jacob and Monod that regulatory networks control gene expression in bacteria ( 1–5 ). Their recognition that expression of a single gene can be repressed by another gene for response to regulatory cues from the environment ranks as one of the top, and now most heavily explored, areas of biology in general and cancer biology. A review in Cancer Research in 1961 by Pitot and Heidelberger not only pays tribute to this pivotal work of Jacob and Monod but with the prescient intent of predicting how the concepts might be woven into our understanding of carcinogenesis ( 6 ). To say their predictions were accurate would be an understatement, as is readily apparent from today's marriage between the exploration of regulation of gene expression and our current efforts to dissect basic mechanisms underlying the origins, initiation, and progression of cancer. It becomes evident as well that the studies of Jacob and Monod, and their implications as visualized by Pitot and Heidelberger, helped usher in a biology that underpins our current quest to evolve new strategies for improving the management of cancer. Hence the selection of the review by Pitot and Heidelberger for inclusion in the current celebration of 75 years of publishing in Cancer Research .

The revelations provided by Jacob and Monod started, as do many great stories in science, with a series of epiphanies by the younger investigator, Jacob, which he brought to conversations with the more established scientist, Monod. They followed their eventual joint excitement over the possibilities raised with a series of experiments, conducted during 1958 through 1961 at the Pasteur Institute in Paris. These resulted in their outlining a model for gene regulation, which survives as a core paradigm today. Their observations established the principle that to properly regulate response of an organism to changing environmental conditions, in specific bacteria for their experiments, a gene circuitry exists wherein one gene product regulates control of another gene. The result is a change in cellular phenotype for cellular metabolism ( 2–5 ). Building on experiments for demonstrating that lambda phage genes can be both induced and repressed in bacteria, the investigators established that changes in need for lactose utilization lead to negative regulation of β-galactosidase ( 2–5 ). The circuitry for this switch formed what is now famously known as the lac operon ( 1–5 ). The studies took advantage of the mating system employed in bacteria, in which the chromosomal material of the male is progressively injected over time into the female, thus progressively carrying genetic material with it. This allowed investigators to map male genes by chromosome position as their entry facilitated gene expression events in the female. Toning down the sexual connotations for the literature, the seminal study of Jacob and Monod, with participation of Arthur Pardee, was first published as a preliminary report in 1958 where it was dubbed the “PaJaMa” experiment ( 1, 3, 5 ). In this study, the investigators were able to show that a gene lacl encoded a trans-acting repressor for the lac gene. In this concept, the activity of the regulator gene is induced when the repressor protein in the cytoplasm is induced by a small molecular weight product generated by the target enzyme. This circuitry paradigm contributes robustly to mechanisms for pathway feedback inhibition.

The nature of the trans-acting molecules through which the repressive process is mediated remained to be determined with many discussions of whether direct DNA–DNA interactions, RNA, proteins, etc., would play this role. These subsequent discussions, held at the headiest of meetings attended by many luminaries in the embryonic field of molecular biology, are credited with leading to the discovery of mRNA as put forth in a review by Alexander Gann ( 3 ). Herein is described a lunch in Sydney Brenner's rooms in King's College on Good Friday, now some 55 years ago, attended by Jacob, Brenner, Francis Crick, Alan Garen, and others where “suddenly that afternoon it became obvious—first to Brenner and Crick, and then to the others present—that the PaJaMa experiment predicted an unstable intermediate in gene expression,” which was concluded to be RNA. This suggested to the attendees that the mediator for the repressor action potentially “really did act at the genetic level controlling production of the unstable mRNA. This discussion, continued that evening at a party at Crick's house, led directly to the experiment by Brenner and Jacob, who, together with Matt Meselson at Caltech that summer, demonstrated the existence of mRNA. Separately, Jim Watson, Wally Gilbert, and Francois Gros arrived at a similar result through different means at Harvard” ( 3 ). The years to come in our current age of biology have revealed that all of the hypotheses derived from the first findings of Jacob and Monod were relevant and presaged the findings of how many different ways such transacting events can be molecularly mediated.

In decades following the above observations, the paradigm of the lac operon and its constituent repressor binding to an operator and inducer ushered in an era, ever growing today, for our understanding of cellular control through signal transduction circuitry and the concepts embodied for heritability of resultant gene expression changes established by epigenetic mechanisms ( 2–4, 7 ). It has been justifiably stated that “few proteins have had such a strong impact on a field as the lac repressor has had in Molecular Biology” ( 2 ). It is hard to imagine, looking back, the degree to which the work of Jacob and Monod would become a knowledge base to build upon in elucidating the vast series of mechanisms used by cells to interpret environmental cues in processes ranging from development to those of adult cell renewing systems challenged by a myriad of normal and abnormal stimuli. A staggering portfolio of cellular machinery to implement these processes continues to unravel in what we now investigate every day as activation of, and heritably transmitting of, information from cell signaling pathways. These include switches in patterns of gene expression and the cell nuclear events that fix these gene events, including looping between DNA regions for control by gene enhancers of promoters, the roles of noncoding RNAs such as long-noncoding and miRNAs, and the roles of DNA methylation, chromatin, and nucleosome positioning in heritably locking in gene expression changes, which can all contribute to creating new cellular phenotypes ( 8 ). Indeed, one may view this as the expansion of, and definition of mechanisms for, the types of gene circuitry proposed and documented by Jacob and Monod.

With the above background in mind, it is remarkable how quickly, and with such prescience, Pitot and Heidelberger brought forth the concepts outlined in their 1961 Cancer Research review ( 6 ). They hypothesized components of the systems outlined by Jacob and Monod could be transposed to a concept of induced phenotypes that are heritably perpetuated and maintained for cellular responses to short, transient exposure to carcinogens ( 6 ). They theorized that ongoing experiments in the carcinogenesis field suggested these above interactions might possibly allow engendering of a malignant cell without necessitating participation of genetic (DNA) changes such as gene mutations. Critical to this proposal, they envisioned a potential state of “reversion” which might allow for changing the malignant phenotype back to the nonmalignant state ( 6 ). These concepts are dear to the heart of researchers on the continuing quest to outline the precise roles for epigenetic alterations in the initiation and progression of cancer and the possibility that targeting such changes, and/or what controls them, could provide for potent cancer management strategies ( 9, 10 ). They perceptively weave the concepts of Jacob and Monod into a possible alternative to the then prevailing doctrine that “cancer may result from a direct interaction of carcinogen with genetic material”—a theory they reasoned had developed by “acceptance by many as the mechanism of carcinogenesis on the basis of theoretical simplicity rather than of scientific data.” As an alternative, Pitot and Heidelberger considered, and deeply modeled, how the findings of Jacob and Monod might lead to the possibility that “a cytoplasmic interaction of a carcinogen and a target protein could lead to a permanently altered and stable metabolic situation without the necessity of any direct interaction of the carcinogen and genetic material” ( 6 ). A critical feature of their hypothesis was that “under the proper circumstances and before chromosomal alterations occurred, the process might be reversed and lead to the production of a normal from a tumor cell.”

In their proposal, via a series of presented complex models, they proposed multiple scenarios and different variations of biochemical and genetic themes that could mediate their proposed interactions, arriving at the following bottom line prediction—that a carcinogen can bind to and interfere with the repressor of a growth process, thus effectively negating function of the repressor through a process of “cytoplasmic inheritance.” Thus, this interference is not dependent on continued presence of the carcinogen in daughter cells as they divide ( 6 ). Clearly, in modern parlance, we visualize these dynamics as proceeding through the cytoplasm to the nucleus via a series of signal transduction events that subsequently get abnormally fixed by epigenetic processes involving DNA methylation, chromatin, and changes in nucleosome position ( 8–10 ). Clearly, this suggests a profound role of epigenetic abnormalities early during cancer initiation and this possibility is the subject of many investigations today ( 9, 10 ). In this regard, Pitot and Heidelberger wisely articulate several key rules, and cautions, inherent to their proposed mechanisms and this wisdom enriches their predictions as they are playing out today. First, they stress that “it must be apparent to the reader that we are here dealing only with the earliest changes in carcinogenesis. Once the altered regulation is established (possibly within minutes or hours), other effects appear, such as aneuploidy, increased glycolysis, apparent multiple enzyme deletions, etc., which are probably secondary to the primary changes” ( 6 ). Second, “it is not our intention to rule out or deny the possibility that chemical carcinogenesis is a consequence of the direct interaction of the compound with genetic material. Rather, it is our purpose to call attention to alternative explanations, based upon current concepts of metabolic regulation and control, that permit the perpetuation of metabolic changes brought about by the temporary interaction of the carcinogen and a cytoplasmic protein” ( 6 ). Finally, they conclude that “by the application of these or similar theoretical models, it is possible to reconcile the large body of sound experimental data on chemical carcinogenesis with current concepts of metabolic regulation, and early cancer could be considered as a phenotypic rather than a genotypic disease” ( 6 ).

In reviewing the work of Jacob and Monod, John Beckwith ( 5 ) provides a wonderful sentiment that might serve also as a coda to the ingenious joining by Pitot and Heidelberger of the lac operon story with the field of human carcinogenesis—“new theories that become successful paradigms for their field, in their initial form at least, do not provide a correct explanation for all of the phenomena that are considered important to that field.” And, yet as implied here, any initial flaws in such theories do not prevent their never being separated from the body of invaluable work they help to spawn. Our understanding today of gene transcription is driving virtually every aspect of basic and translational tumor biology, again reminding us of our ride on the shoulders of those coming before. The publication by Pitot and Heidelberger is, then, emblematic of why we are celebrating 75 years of publishing in Cancer Research .

No potential conflicts of interest were disclosed.

• Metabolic Regulatory Circuits and Carcinogenesis

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Operon Concept, Jacob–Monod Model

The operon concept states that the set of genes that are transcribed in the prokaryotes are under the control of operons. Jacob and Monod showed the organization of bacterial genes into operons.

In bacteria and  archaea , structural proteins with related functions are usually encoded together within the genome in a block called an  operon  and are transcribed together under the control of a single  promoter , resulting in the formation of a polycistronic transcript. In this way, regulation of the transcription of all of the structural genes encoding the enzymes that catalyze the many steps in a single biochemical pathway can be controlled simultaneously, because they will either all be needed at the same time, or none will be needed. For example, in E. coli , all of the structural genes that encode enzymes needed to use lactose as an energy source lie next to each other in the lactose (or  lac ) operon under the control of a single promoter, the  lac  promoter.

French scientists François Jacob (1920–2013) and Jacques Monod at the Pasteur Institute were the first to show the organization of bacterial genes into operons, through their studies on the  lac  operon of  E. coli . For this work, they won the Nobel Prize in Physiology or Medicine in 1965. Although eukaryotic genes are not organized into operons, prokaryotic operons are excellent models for learning about gene regulation generally. There are some gene clusters in eukaryotes that function similarly to operons. Many of the principles can be applied to eukaryotic systems and contribute to our understanding of changes in gene expression in eukaryotes that can result in pathological changes such as cancer.

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• Regulation of the lac operon

MCAT Official Prep (AAMC)

Practice Exam 3 B/B Section Passage 4 Question 18

Sample Test B/B Section Question 29

• Gene expression in prokaryotes is largely regulated at the point of transcription. Gene expression in eukaryotes is additionally regulated post-transcriptionally.

• Prokaryotic structural genes of related function are often organized into operons, all controlled by transcription from a single promoter. The regulatory region of an operon includes the promoter itself and the region surrounding the promoter to which transcription factors can bind to influence transcription.

• Jacob and Monod gave the model to explain the organization of genes into operons that control the transcription in prokaryotes. They were awarded Nobel prize for this.

operon : a unit of genetic material that functions in a coordinated manner using an operator, a promoter, and structural genes that are transcribed together

promoter : the section of DNA that controls the initiation of RNA transcription

polycistronic : mRNA that can encode for multiple polypeptides

archaea:  are single-celled microorganisms with a structure similar to bacteria

lac operon: The lac operon is an operon that encodes proteins that allow the bacteria to use lactose as an energy source

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Classic Spotlight: the Birth of the Transcriptional Activator

In the famous “PaJaMo” experiment, Arthur Pardee, Francois Jacob, and Jacques Monod exploited the technique of diploid analysis to show that a repressor controlled expression of the Lac operon. Loss-of-function (recessive) mutations in the lacI gene confer a constitutive phenotype ( 1 ). Subsequently (for a review, see reference 2 ), it was shown that lacI mutations that destroy the inducer binding site (superrepressor, I S ) confer a dominant, noninducible phenotype and that the repressor turns off expression by binding a site, called the operator, that was defined by cis -dominant constitutive mutations (O C ). Because the repressor model was so elegantly simple and it offered satisfying explanations for regulatory systems as seemingly diverse as bacteriophage λ, negative control by a repressor soon became generally accepted as the universal model of gene regulation.

Ellis Englesberg was the first to challenge the universal nature of negative control with his studies of the arabinose operon. In a classic Journal of Bacteriology paper ( 3 ), Englesberg et al. used diploid analysis to show that araC mutations that confer a noninducible phenotype cannot be I S -like because they are recessive. This result suggests that the product of the araC gene is needed to turn on the ara operon, and the authors coined the name “activator” to emphasize the role of this protein in positive control.

Englesberg et al. ( 3 ) also isolated constitutive mutations and showed that they were not O C -like because they were not cis dominant; they mapped to araC ( araC C ) and could complement araC null mutations in trans . However, a complication emerged with the discovery that the araC C mutations were recessive to araC + . This should not be the case for a regulatory protein that functioned in a purely positive fashion. To account for this complication, Englesberg et al. proposed an additional twist to the Lac model. In the absence of inducer, LacI binds the operator and represses expression; the inducer allosterically changes the conformation of LacI to an inactive form. Like LacI, AraC exists in two conformations. However, in contrast to LacI, both conformations of AraC are active; in the absence of inducer AraC acts as a repressor, and in the presence of inducer it acts as an activator to stimulate expression. The araC C mutation is recessive because repression is epistatic to activation.

The model presented in the Englesberg et al. paper ( 3 ) has withstood the test of time and is basically correct. However, partly because of the fact that AraC did function as a repressor and partly because of vociferous resistance to the concept of positive control from influential scientists such as Monod, it would take Englesberg several more years and the accumulation of overwhelming evidence that there was no LacI-like repressor in the Ara system before his model and the concept of activators were generally accepted. Ironically, activators turn out to be far more common in eukaryotes than repressors.

The views expressed in this Editorial do not necessarily reflect the views of the journal or of ASM.

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Jacob, Monod, the Lac Operon, and the PaJaMa Experiment-Gene Expression Circuitry Changing the Face of Cancer Research

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• 1 The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland. [email protected].
• PMID: 27197249
• DOI: 10.1158/0008-5472.CAN-16-0865

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Jacob-Monod model

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The theory postulated by the French biologists F. Jacob (1920– ) and J. Monod (1910–76) in 1961 to explain the control of gene expression in bacteria (see operon). Jacob and Monod investigated the expression of the gene that codes for the enzyme β-galactosidase, which breaks down lactose; the operon that regulates lactose metabolism is called the lac operon.

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The nobel prize in physiology or medicine 1965.

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François Jacob

Prize share: 1/3

André Lwoff

Jacques Monod

The Nobel Prize in Physiology or Medicine 1965 was awarded jointly to François Jacob, André Lwoff and Jacques Monod "for their discoveries concerning genetic control of enzyme and virus synthesis"

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Discovering the lac operon, François Jacob

• Description

Interviewee: François Jacob. François Jacob talks about bacterial mutants that could not metabolize lactose. Using these mutants, Jacob and Monod figured out how protein production is controlled. (DNAi Location: Code > Controlling the code > Players > François Jacob and Jacques Monod > Making mutants)

Well, Monod started to make mutants, he made mutants which were unable to use lactose, that is to eat lactose and to metabolize lactose, and he showed that in these, some of these mutant there was no galactosidase made. So, that was a gene, which controlled the synthesis of galactosidase. Then they found also that there was another gene closely adjacent, which turned out to be adjacent to the first one, which had to do with the entry of lactose in the cell, and they called that permease. So, bacteria could become unable to utilize lactose, either because they were unable to make the enzyme, which cut the lactose, or because they became unable to concentrate lactose in the cell. In addition, in most wild type E. coli , that is the E. coli you find in nature or in the guts of all of us, the enzyme is inducible as we said, that is, it's made only in the presence of galactoside. But they also found, the Monod group found that there are mutants, which are able to make the enzyme without the galactoside. So the first one, which is the normal, we are call inducible, and the other one was called constitutive. And the question was, why is it constitutive?

lac operon,jacob and monod,bacterial mutants,jacques monod,franis,protein production,galactosidase,dnai,location code,constitutive,interviewee,e coli,glucose,guts,bacteria,synthesis,presence

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