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PREAMBLE: Before there is debate, let me preface this question by stating that I am indeed aware of the question Why do replicants have a short lifespan? However, none of its answers adequately answer my question below, and I believe the spirit of the question is entirely different. (That question is asking for the motivation behind giving the replicants a short lifespan, not about how the short lifespan is achieved.)

 


 

In Blade Runner, Roy, Pris, Leon, and Zhora — replicants manufactured by the Tyrell Corporation — suffer from "accelerated decrepitude", to quote Pris. These particular replicants have a four-year lifespan.

In the Blade Runner universe, replicants are synthetic lifeforms that include genetically-engineered organic components, such as skin, hair, and eyes. These are grown according to custom genetic patterns supplied by the Tyrell Corporation. (In the film, we see that eye production is outsourced, for instance. The character Hannibal Chew grows eyes for replicants in development.)

The conversation between Tyrell and Roy suggests the lifespan problem is biological in nature:

TYRELL: The facts of life. To make an alteration in the evolvment of an organic life system is fatal. A coding sequence cannot be revised once it's been established.

When pressed for more information, Tyrell explains:

Because by the second day of incubation, any cells that have undergone reversion mutations give rise to revertant colonies like rats leaving a sinking ship. Then the ship sinks.

After Batty offers a different possible solution, Tyrell counters with:

...but it does give rise to an error in replication so that the newly-formed DNA strand carries the mutation....

Assuming Tyrell is telling the truth, then there is a natural question:

Is Tyrell's explanation indicative of exceptionally short telomeres in the cells of replicants?

The types of problems regarding life extension put forward by Tyrell would support this. One way to combat the telomere length problem would be to use telomerase to protect nucleotides on chromatids. However, this would theoretically leave the subject open to opportunistic malignancies resulting from mutated cells that form stable colonies due to reduced cell apoptosis.

Is this what Tyrell is describing?

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    Note to potential answers: This site is for answering questions about fictional works based on the work itself. Please stay away from any speculation about "how it works in real life", as that is off-topic. – KutuluMike Feb 21 '15 at 22:11
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    There appear to be two issues with this question; 1) Despite your protestations, it's largely a dupe and 2) You seem to be asking for a scientific explanation. I'm happy to see where this goes, but I suspect this is going to end up getting closed unless you can address these problems. – Valorum Feb 21 '15 at 22:17
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    @Richard : I disagree with the word "largely" (the other question asks for the motivation behind giving the replicants a short lifespan, not about how the short lifespan is achieved). I've tried to tighten up the question so that it is more about the actual work. – Praxis Feb 21 '15 at 22:32
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    @Praxis I had no problem with the question, I'm merely warning those who want to post an answer to stick to material that's present in the movie, or at least the book, and not their college biology textbook. – KutuluMike Feb 21 '15 at 22:42
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    @Michael Edenfield--the rules don't forbid people to talk about how some specific bit of a science fiction work relates to real-world science--the rule is that "Questions seeking scientific solutions or explanations are off-topic unless they relate directly to a cited work of fiction". So I think a question of the type "is this dialogue in a SF work based on real scientific theories, and if so which ones?" is fine to ask here. – Hypnosifl Feb 21 '15 at 23:48
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Pretty sure the explanation is just technobabble, with no coherent rationale for why their lifespans couldn't be extended in terms of any real-world science, telomeres or otherwise. Someone asked a question about the science in Tyrell's dialogue on quora.com here, and got one answer from "Joshua Engel" saying "Well... ethyl methyl sulfone is an alkylating agent, and it is mutagenic. ... The rest is gibberish", followed by a much more detailed answer from "Zachary Williams, Graduate Student, Molecular Microbiology, Tufts University" which I'll just quote in full:

As Joshua said, the rest is gibberish, but there are different levels of gibberish, i.e., some parts are just wrong, and other parts could be characterized as "not even wrong."

1: " To make an alteration in the evolvement of an organic life system is fatal. A coding sequence cannot be revised once it's been established."

Common misconception. The vast majority of possible point mutations in the human genome are very close to neutral in their effect on phenotype (i.e., observable changes in organismal form and function). There are a number of reasons for this:

First, most of the human genome is...well, I will not say "non-functional," 'cause that would piss some people off, so, instead, I'll say, rather, that any potential function is not constrained by sequence. Maybe it's a spacer or has some global structural significance (a la centromeres), but it shows no signs of purifying selection. You can google the Encode controversy if you want to get way more reading material than you could ever finish on this topic... Anyway. Also a lot of it is clearly derived from transposons and/or viruses, and while such sequences can be co-opted by evolution to serve some function, most of them are pretty clearly not. For one, all the genes tend to be mutated and deleted all over the place. Also, you see little islands in the genome where a number of unrelated transposons and/or endogenous viruses are crammed together, which I like to think of as "islands of no selection," where any old DNA sequence can jump in with no consequences to the host, leading to an accumulation of junk, over many many generations.

Second, for protein coding sequences, most single point mutations are close to neutral, either because the change in DNA sequence does not change the actual amino acid sequence (google genetic code degeneracy), or the amino acid coded for by the mutation is sufficiently similar chemically and biophysically to the wild type aa, or the amino acid in question is simply not very important to the protein's function. A really interesting paper on this came out recently: http://www.ncbi.nlm.nih.gov/pubmed/23041932 They mutated every amino acid in a certain protein to every other amino acid, and characterized the changes in function. Most mutations had little to no effect.

Thirdly, other reasons but I'm tired of this.

  1. "Because by the second day of incubation, any cells that have undergone reversion mutations give rise to revertant colonies like rats leaving a sinking ship. Then the ship sinks."

Um...no idea. Those are all sciencey words, yes. Reversion mutations are a real thing. Revertant colonies are a real thing. Incubation is a real thing. But the sentences convey no meaning to me.

  1. "EMS recombination"

Not a real thing AFAIK. EMS causes point mutations, not recombination.

4."It created a virus so lethal the subject was dead before he left the table."

No. Maaaaybe they were thinking of DNA methylation, rather than alkylation. Methylation of certain sites on DNA is a very important form of genetic regulation. The virus angle comes in because methylation can silence gene expression, and it appears that one important role of this is silencing viruses that have inserted their DNA into ours (google endogenous retroviruses, my favorite things in the whole world). So, theoretically, a de-methylating agent of some sort could reactivate a dormant provirus, causing Bad Things. Or good things; people are currently trying to use this as a way to cure HIV, by reactivating latent HIV in cells so that anti-HIV drugs can kill it.

  1. "Then a repressive protein that blocks the operating cells."

Repressor proteins are a thing, yes. Not sure what they have to do with...whatever the topic is, which I'm not really clear on. Operating cells: no idea.

  1. "Wouldn't obstruct replication, but it does give rise to an error in replication so that the newly formed DNA strand carries the mutation and you've got a virus again."

Hrm. Yeah, no clear meaning to me. Not even wrong.

The end.

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    Dude. That was awesome. Way more effort than a few lines in movie deserve, but awesome none the less. – WhatRoughBeast Feb 21 '15 at 23:06
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    +1 I'm an absolute fan of Blade Runner, to the point I sometimes consider it my favorite movie EVER, but Tyrell's explanation bothers me every time I re-watch the movie. It's obviously technobabble even to a layman like myself. I wish they had replaced it with more hand-waving (which is always acceptable in SF) and fewer obviously misused actual technical words. – Andres F. Feb 22 '15 at 1:36
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    @Andres F. -- Yeah, I always felt the same way...the part that sounded most silly to me as a layman was the idea that a "potent mutagen" applied to replicant DNA could somehow lead to the creation of a lethal virus, although the comment by Zachary Williams on this above actually suggests it's slightly less crazy than it sounds because a human genome can contain dormant provirus code...still seems like a huge stretch that this would be the inevitable result of some form of genetic engineering, as opposed to a freak accident. – Hypnosifl Feb 22 '15 at 3:55
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The Tyrell speech about replication errors and viruses was invented for the Blade Runner film. The novel Do Androids Dream of Electric Sheep simply points out that android metabolism is faster than human metabolism and that androids die because of poor to nonexistent cell replacement. Basically, like any machine with moving parts that aren't replaced, they wear out.

RACHAEL:“They never could solve that problem. I mean cell replacement. Perpetual or anyhow semi-perpetual renewal. Well, so it goes.”

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