It seems like there has been more hype around synthetic biology in the tech press the last year or so, but it still feels like this field is being slept on a bit. AGI gets a lot of press but is at best decades out, however one could argue that the potential (for good and bad) of synbio is close to as large, but the tech is much more real. In many cases it already exists -- we can modify human embryos, the first human study of CRISPR in the US kicked off a few weeks ago -- and in others it doesn't seem too far out
I'm a non scientist and have been excited to learn more about this field, but to find out the most exciting stuff you need to read scientific papers. The details are the coolest parts IMO. A bit of self promo here, but I recently wrote a blog post summarizing a Stanford synbio paper in layman's terms [0].
(Full disclosure, i run a YC startup selling to synbio + think that it's undervalued)
The field really doesn't do blog posts, it's a shame.
For some interesting stuff in synbio that's approachable to your prototypical HNer, check out [1], a Verilog-to-DNA compiler that works with small logic circuits. [2] (Not really synbio) but using reed solomon codes to better do High-Throughput Screening. [3] PACE, a way to ask evolution to implement a particle filter for us. [4] A remapping of the base pair 3-tuple to amino acid that maximizes edit distance, filling in the gaps with STOP codons - stopping something from evolving, and [5] some cool people working on wholly synthetic cells.
[1] Nielsen, A. A. K., Der, B. S., Shin, J., Vaidyanathan, P., Paralanov, V., Strychalski, E. A., … Voigt, C. A. (2016). Genetic circuit design automation. Science, 352(6281). https://doi.org/10.1126/science.aac7341
[2] Erlich, Y., Gilbert, A., Ngo, H., Rudra, A., Thierry-Mieg, N., Wootters, M., … Zuk, O. (2015). Biological screens from linear codes: theory and tools. BioRxiv, I(1), 35352.
[3] Dickinson, B. C., Leconte, A. M., Allen, B., Esvelt, K. M., & Liu, D. R. (2013). Experimental interrogation of the path dependence and stochasticity of protein evolution using phage-assisted continuous evolution. Proceedings of the National Academy of Sciences, 110(22), 9007–9012.
https://doi.org/10.1073/pnas.1220670110
Esvelt, K. M., Carlson, J. C., & Liu, D. R. (2011). A system for the continuous directed evolution of biomolecules. Nature, 472(7344), 499–503. https://doi.org/10.1038/nature09929
>AGI gets a lot of press
Does it?
Yes AGI in sci-fi (e.g matrix) is not new.
But the medias and even the AI journals do almost 0 press about AGI.
Narrow (specialized) AI is now mainstream, especially the deep learning paradigm.
But clearly solving an NLP task is not building an AGI.. At best it's solving a constituent of an AGI.
But many constituents of an AGI does not have an NLP task, which means mostly nobody work on it.
An AGI, to be implemented need a big, sound, cognitive architecture.
AGI gets a lot of press
So, can you name at least one AGI architecture?
Nobody knows nor talk about them. To name the two most promising:
Cyc and opencog.
https://www.google.com/url?sa=t&source=web&rct=j&url=https:/...
Well currently the website is down... But it is enlightening to read such an architecture.
I'm no biologist, but I think you're missing some causes of aging.
DNA isn't the only thing that has to stay mutation free for an organism to not age. Lots of the cellular machinery will propagate error to future generations. For a simple example see prion diseases. Sure they seem big scary and rare, but I'd suspect in reality this sort of thing happens way more often than we probably realize just in ways that can't be spread person to person even via cannibalism or that has much lower consequences.
Keep in mind also that ending aging is striving against not just entropy but evolution. Cancer cells are selected for. Obviously not on a species level, but if even just one cell messes and starts reproducing out of control it will quickly take over. You can implement more checks along the way and repair damage as it comes up, but the point remains that if even just one cell somehow isn't effected, it will be selected for among all the cells that make you up.
Another thing that I identify as contributing to aging other than cell DNA is mitochondrial DNA (it's weird to realize we have two different DNA in each cells)
Does other organelles apply?
I fking don't know and how could I? :(
Prion pathophysiology isn't completely understood, and there's some literature to suggest certain types are caused by environmental factors.
Regardless, curing cell aging is only the first step in "curing" aging. Some cell types simply stop dividing as a natural part of the lifecycle, and it isn't necessarily telomere related.
Additionally, the only cells that don't shorten telomeres over time are cancer cells. Aging is a complicated process we don't understand.
Aging is a complicated process we don't understand.
I mostly disagree, while it is unknown how much of ageing is not a cause of DNA damage, I expect by far most of it come from DNA damage.
Btw: are organelles just protein complexes?
If so organelles are made by DNA too.
The hayflick limit isn't the only cause of senescence. There are many biochemical processes that can induce senescence, and a variety of reasons the cell might do that. Oncogenic stress from reactive oxygen species, double stranded DNA breaks, enzymes like p53 tumor suppressor (this is a big one) and histone deacetylase inhibitors can all lead to senescence.
Also, the hayflick limit has little to do with DNA damage per se, but rather is about telomere shortening. DNA is replicated in a ssomewhat asymmetrical fashion, and at the end of the chromosome, and needs the telomere to act as a buffer. Eventually you run out of buffer because every replication loses a little bit. But there's no innate damage to the DNA related to telomere shortening - all of the generic code still is maintained.
>Btw: are organelles just protein complexes? If so organelles are made by DNA too.
No... Not even close. There are some proteins in them and proteins interact with them but organelles are extremely complex. They are structures made of lipids, proteins, minerals, RNA, etc.
I read over it. Interesting. This is something I've been looking into a lot. THe idea to use crisper to alter the dna is good, but the tech isn't perfect and you could in fact program in unintended mutations.
That's why they have to run through a lot of source material before they get the right dna cuts they one, then they isolate those strands and let them proliferate.
You can also have your body clean up the older/damaged cells via autophagy.
Honestly I feel that epigenetics will be the answer to ending aging. Since the body is capable of producing new stem cells all you would have to do is map out the genetic triggers for creating those to replace older cells, and instigating autophagy to clean out the garbage.
For instance, with skin, the "aging" saggy, wrinkly, thinning skin is a result of the body no longer producing enough elastin, and collagen deficiency.
People believe that it's natural for the body to stop elastin production, but I've seen studies where scientists were able to trigger the genes in the dna that're responsible for creating the stuff needed to create elastin.
The cells were perfectly healthy, they simply stopped producing elastin, but when you introduce the trigger compound into the system the genes react to the trigger and you get elastin production.
If you can't pinpoint one gene that goes inactive in the dna that's the sole cause of aging, simply keep replacing damaged genes with fresh ones, and then piecemeal activate any inactive genes necessary to maintain a certain biological age.
So you could have a chronological age of say, 1,000 but your biological age is twenty.
I found this page because I have a google alert set up for "synthetic biology" I have no idea what this website is about honestly.
Exchanging emails or contact info on a public site would be a bit crazy, but I'd love to talk to you about this more. I'm not planning to just theorize about this. I eventually want to get my own lab and put in some work!
Ethics are a good reason to postpone research in a certain direction. However, the frightening part is that countries with lower ethical standards can still do whatever they want and over time even gain a technological advantage over the US. We need to figure out how to deal with this.
Ethics is absolutely not an argument to postpone any kind of research. It does not solve the problem, it just hides it under a rug, essentially creating two problem out of one.
Why doesn't "ethics" account deaths caused by not allowing human DNA editing?
Ethics is not a complex thing despite what most people believe. Utilitarism is scientifical ethics.
I'm a non scientist and have been excited to learn more about this field, but to find out the most exciting stuff you need to read scientific papers. The details are the coolest parts IMO. A bit of self promo here, but I recently wrote a blog post summarizing a Stanford synbio paper in layman's terms [0].
[0] https://www.baybridgebio.com/blog/synbio-laymans-terms.html