Biophysicists Consider Tumor Suppressor Protein 53 To Be A Dimmer Switch

Protein p53 with DNA

Protein p53 with DNA

Protein 53 (or tumor protein 53), is a tumor suppressor protein that in humans is encoded by the TP53 gene.  Since 2003, biophysicists have referenced this protein 53 (p53) to be a rheostat, or dimmer switch in laymen terms.  Although this terminology is only meant to be a metaphor, there is much validity to the fact that p53 functions exactly as a dimmer switch.  Ongoing examination of p53 indicates that it does more than operate as an on/off switch, but regulates ranges of values that are fine-tuned as needed in the cell. 

Molecular Rheostats Control Expression of Genes

In 2003, a review paper published in the January 10 edition of Cell, entitled “Regulating the Regulators: Lysine Modifications Make Their Mark,” stated in the abstract:

Although the composition of this machinery is largely known, mechanisms regulating its activity by covalent modification are just coming into focus.  Here, we review several cases of ubiquitination, sumoylation, and acetylation that link specific covalent modification of the transcriptional apparatus to their regulatory function. We propose that potential cascades of modifications serve as molecular rheostats that fine-tune the control of transcription in diverse organisms [The emphasis is mine].

In their 2003 review paper, Richard Freiman of Howard Hughes Medical Institute and Robert Tijian of UC Berkeley itemize numerous examples of how molecular systems regulate genes.  The paper employs vocabulary terms such as “elaborate,” “intricate,” “exquisite,” and “dramatic.”

The paper begins by asserting the following:

The temporal and spatial control of gene expression is one of the most fundamental processes in biology, and we now realize that it encompasses many layers of complexity and intricate mechanisms. To begin understanding this process, researchers have identified and partly characterized the elaborate molecular apparatus responsible for executing the control of gene expression [emphasis mine].

The paper further describes molecular rheostat function, “The molecular machinery responsible for controlling transcription by RNA polymerase II (RNA pol II) is considerably more complex than anyone had anticipated.” [Emphasis added].  The Freiman and Tjian (2003) paper continues:

“It is not hard to envision that these lysine residues therefore serve as critical molecular switches that can respond to different signals in highly specific ways. In addition, since most proteins contain many lysine residues, transcription factors may undergo multiple modifications simultaneously or in sequential order, pointing to the possibility of generating complex networks of regulatory events.” [Emphasis mine]

Therefore, the Freiman and Tjian (2003) paper concludes:

“Clearly, transcription is exquisitely regulated in all organisms, and one mechanism utilized to achieve such regulation is covalent modification of the transcriptional machinery.  Future studies in diverse organisms and specialized regulatory pathways should further illuminate how transcription factor modification contributes to the elaborate mechanisms of gene regulation.”

Molecular Rheostats In Tadpole Spinal Cord Development

A fresh new research paper just hot off the press is Zhang, Issberner and Sullar, “Development of a spinal locomotor rheostat,” PNAS June 27, 2011, published online before print June 27, 2011, doi: 10.1073/pnas.1018512108.  In Zhang et al (2011), Scottish scientists examining Xenopus tadpole spinal cord development found that the first pools of neurons are all alike.  The neurons rapidly sort out into ventral and dorsal domains within a day.  During tadpole development, the neurons become more specialized as the tadpole requires increased need to swim with greater finesse.

The Zhang et al (2011) PNAS paper reads:

“This unfolding developmental plan, which occurs in the absence of movement, probably equips the organism with the neuronal substrate to bend, pitch, roll, and accelerate during swimming in ways that will be important for survival during the period of free-swimming larval life that ensues. [Emphasis mine]

It is very difficult to avoid inferring from this quote that tadpole development features foresight as to what the tadpole will need, and fine-tunes the “rheostat” of neural specialization to permit the tadpole to interact with its environment.

Protein p53 Acts as a Dimmer Switch

Protein p53 Can Act As A Dimmer Switch Controlling Cell Suicide

Molecular Rheostats In Humans

Medical Express just recently reported that scientists at the Salk Institute for Biological Studies have found clues to the functioning of an important damage response protein in cells. The protein, p53, can cause cells to stop dividing or even to commit suicide when they show signs of DNA damage.  Protein 53 is responsible for much of the tissue destruction that follows exposure to ionizing radiation or DNA-damaging drugs such as the ones commonly used for cancer therapy.

p53 (green) is a tumor suppressor

The tumor suppressor protein p53 (green) and its regulator Mdm2 (red) are shown in breast cancer cells using fluorescent tags.

Geoffrey M. Wahl, professor in the Salk Institute’s Gene Expression Laboratory, describes p53 is “… like a dimmer switch, or rheostat, that helps control the level of p53 activity in a critical stem cell population and the offspring they generate.”  Professor Wahl is the senior author of the study, which appears online in the journal Genes & Development on July 1, 2011. “In principle, controlling this switch with drugs could reduce the unwanted effects from DNA-damaging chemotherapy or radiation treatment, allowing higher doses to be used.”

The regulator protein p53 is a decision maker concern DNA repairs. Protein 53 decides whether repairs should proceed.  If not, p53 commands the affected cell to commit suicide.  Now, how’s that for intelligent design!  The Salk Institute findings show “that a short segment on p53 is needed to fine-tune the protein’s activity in blood-forming stem cells and their progeny after they incur DNA damage [emphasis mine].”

The article notes that short segment is “an evolutionarily conserved regulatory segment of p53.” The term “conserved” is the word biologists use to reference a process that started out fully functioning and perfectly developed in its advanced state initially at the beginning of life, and since then has never evolved.

The Medical Express article goes on to say this about protein 53:

“One problem with p53 is that it apparently evolved to protect the integrity of the genome for future generations, rather than to prolong the lives of individual cells or animals. From the point of view of an animal, p53 sometimes goes too far in killing cells or suppressing growth.” [Emphasis mine].

Excuse me?  Did the medical science journalist just say “evolve to”? Someone needs to remind Darwinists every once in a while that evolution does not evolve “to” do anything.  Natural processes are supposed to be entirely unguided, and to suggest there is foresight implies teleology.  Darwinists continue to remind each other that they need to quit using teleonomic language, but I suppose it is difficult mental gymnastics at times to avoid invoking intelligent design.

The existence of molecular rheostats and dimmer switches that fine-tune processes says nothing about how they came into existence and became fine-tuned.  The only rheostats and dimmer switches we know about, even if they are broken ones, are intelligently designed. 

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2 Responses to Biophysicists Consider Tumor Suppressor Protein 53 To Be A Dimmer Switch

  1. sholto david says:

    Using language that appears to invoke intelligent design is convenient. Of course it would have been possible to say that:

    “Previous organisms existed without the protein p53, by some genetic duplication/divergence/mutation event the p53 gene appeared and p53 protein came into existence, the effect p53 had on the cell was to cause it to die upon DNA damage (no one is suggesting that a perfect mechanism came into existance the first time p53 was transcribed, over time the function of p53 was refined by the process of mutation and natural selection), since all cells in the organism share the same DNA and a single cancerous cell could destroy them all by causing death in the organism the net effect of p53 was conservation of the organisms DNA, in accordance with the idea of natural selection this organism would be better placed to proliferate and replace its competitors since its chance of death by cancer has been reduced its reproductive potential has been increased…”

    You don’t need to invoke the language of intelligent design but it is convenient because as humans we live in a largely designed/created (by man) world. When trying to explain some concept to another human it is convenient to communicate in terms of purpose and design, because that is what we do best. As scientists we have a common understanding that we don’t actually take this to mean that the p53 gene was created by supernatural forces. When I tell you that my brain hurts reading your blog it doesn’t literally mean that I am experiencing the sensation of pain in my skull, it just means that I find what you are writing dumb. By all means attack the theory of evolution on a scientific basis if you must, at least in some ways it is entertaining, but by picking at the language a scientist would use you are merely being deceptive and disingenuous to your readers.

  2. David, I greatly appreciate your comments, which are very welcome.

    You commented, “You don’t need to invoke the language of intelligent design,” but I am not sure exactly where it was invoked. You pasted a paragraph from the article, but I didn’t see where ID was invoked in that quote. As such, there’s nothing available for me to reply to. If you could direct my attention to the content you find objectionable, then we would have something tangible to discuss.

    You wrote, “As scientists we have a common understanding that we don’t actually take this to mean that the p53 gene was created by supernatural forces.” I agree with you 100%. However, what mystifies me is that you seem to imply that my article suggests creation or supernatural speculation, of which I most assuredly can tell you that there is no content in this article that should lead anyone to any such idea. I don’t know what content there is in this essay that would cause you to draw the conclusion of invoking any metaphysical contemplation. Please write back and identify whatever content you believe is scientifically objectionable. I don’t see how your comment pertains any relevance to my article. I’m failing to see a connection.

    You also advised, “By all means attack the theory of evolution on a scientific basis if you must.” But, why? I accept the theory of evolution. Why would I attack it? There are many scientists already challenging existing hypotheses involving evolutionary theory, and I am very much okay with the process as it is performed presently. If you think I have challenged evolutionary theory, please explain so I can follow your logic.

    And, you then conclude, “… by picking at the language a scientist would use you are merely being but by picking at the language a scientist would use you are merely being deceptive and disingenuous to your readers to your readers.” How is scientific data deceptive? You seem to be claiming that somehow the content in this article is “deceptive and disingenuous,” but you didn’t offer any reasons for this comment. I would like to know upon what basis you would assert this concern. No one I know of would ever desire to be “deceptive and disingenuous,” and I certainly do not want to misleading. So, if you could please write back and let me know what the problem seems to be, I would greatly appreciate it so that I can edit whatever content is objectionable, and clear up anything that could be the source of confusion.

    Thanks again for your comments, they are most appreciated.

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