RandomJ wrote:Some more on the pathogen, now with more details on PC, AC, UV and SIP defense.
"Normal" biopolymer structures intended for detection of hostile (proteolytic enzymes, acids, etc) environments, substrate attachment, interbacterial interaction (biofilm formation) and nutrient processing (aggression against large biopolymer structures, be that proteins, lipids, polysaccharides or combinations of them) will be integrated into the polymer wall using several methods (often trans-membrane anchors), resembling the S-Layer complex.
Several structures will be intended specifically for detecting unfriendly (phagocytic) environments. Upon discovering an unfriendly environment, the pathogen will enact several countermeasures, including enacting active countermeasure protein complexes that rapidly dump H+ and Cl-, and complexes that rapidly form superoxide in the environment (
dear immunocyte, please lyze yourself!).
After dumping the payload, the defense complexes shut down and will eventually rotate out.
Afterwards, measures are taken to decrease permeability of UHMWPE structure and prevent anything from getting past it (seal shut what you can seal shut), and initiating metabolic hibernation (you can not go on long enough while being sealed shut in a plastic bag, so you really want to decrease your metabolism to wait it out).
If there is no indication of improvement in external environment, where attempts to restore the S-complex like structures fails, with permeability-creating structures being repeatedly destroyed, ATP and reserve materials depleting and internal metabolic waste level rising (a situation our Little Boy will find itself in if it encounters a very resilient and persistent alien phagocyte), the pathogen will rapidly form a very resilient endospore.
Endospore formation is also immediately triggered by exposure to high temperature (sufficient to disrupt UHMWPE synethesis), overwhelming UV, chemically aggressive environment, sudden decrease in temperature, irradiation, or any combination of those.
Endospore takes advantage of LB’s unique UHMWPE complexes, and uses additional reinforcement of exosporium and upper spore coat through mineralized phosphate and sulphate compounds, which provides good defense against chemical, thermal, UV abuse, and even some degree of ionizing radiation protection. Genome will be stored with twofold redundancy, stabilized by binding with chromatinoid protective proteins and dipicolinate compounds.
The LB endospores are unique in that a kind of rudimentary metabolism is activated when a barrage of high-energy radiation is present – melanin-based high-energy particle absorbent complexes are located right under the mineralized layer, catching some of the particles that manage to get through the heavily mineralized shell, and using the energy acquired to power specific dependant antioxidant and shaperone complexes, thus, high energy radiation powers some of the mechanisms intended to counteract it.
Additional protection of the endospore core material will be attained through various redundant antioxidant and shaperone complexes a-la those found in many polyextremophiles, and present only in Little Boy’s endospores and never active in vegetative forms (to avoid conflicts with normal metabolism)
Upon formation of endospore, special purpose lytic enzyme complexes targeting the cell wall UHMWPE are activated, thus ensuring that endospore does not end up “in a bag” and can rapidly respond to a favorable change in environment.
Such a spore will be quite resistant to standard autoclave treatment, with above 98% survival when treated as per standard 20cen Erth sterilization procedure. More hardcore modes, like 134° C for 18 minutes, are barely survivable, with over 80% of spores inactivated, and 23 minutes on 130C guarantee sterilization (
holds true for autoclave and like ONLY, burning an infected forest with napalm will achieve nothing, except maybe additional propagation of viable spores through airborne soot particles)
The endospore shall easily survive formidable ionizing radiation (4000-4900 Gy), extreme cold (indefinite storage in liquid nitrogen) fumigating nitric acid bath, and many, many other horrible things.
Endospores can be stored almost indefinitely.
The major drawback
relatively slow activation of endospore – this super-tough nut has hard time detecting favorable environment change (however, environments typical of living hosts will trigger re-activation and germination in 36-48 hours).
To facilitate endosporal response, the pathogens, when in favorable, nutrient rich conditions, will devote some resources to form an endospore that they will carry around indefinitely. Upon mitosis, one of the daughter cells inherits the spore, the sporeless cell proceeds to (relatively rapidly) spawn a sporeless generation. Daughter cells of sporeless generation will form a “backup spore” as the first cell did, if resources are plentiful. Endospore formation can be halted and resumed in response to various combinations of external circumstances.
While this approach somewhat hinders growth rates, it greatly improves overall resilience (a good part of a healthy colony will have spores hidden inside the vegetative cells “just in case someone tries to rapidly heat it to 130C”)
Which means that the LB will be very hard to kill with fire.
UV/Rad defense in vegetative forms
To protect the vegetative form against UV and rads, melanin-based “radiation sink” functional protein complexes are produced, primarily in the periplasmic space. Producing (and breaking down) melanin in periplasmic space spatially compartmentalizes the noxious process, thus preventing the negative effects on cell growth and reproduction associated with melanin production and breakdown. Upon capturing energetic particles (be that UV or gamma), the melanin “sinks” dump electrons into dedicated NADP/NADPH electron transfer chain via dedicated transmembrane protein links.
The advantage of having those is fourfold:
1) Vegetative form protected against UV directly by preventing damage to the important structures and formation of free radicals
2) Vegetative form protected against ionizing radiation directly by preventing damage to the important structures and formation of free radicals
3) The electron transfer chain for the sinks is dedicated, and thus its very activation is a signaling mechanism for specific rad/UV hazard detection
4) Produces energy from the hazardous environment.
The third and fourth points in the list actually allow for “hardcore”,
D. Radiodurans-style ATP hungry rapid DNA reparation and antioxidant systems to immediately activate upon encounter with radiation hazard. The metabolic toll will be minimal (as the very radiation we counteract gives us some additional ATP) and the ATP hungry “super-reparation” and “super-antioxidant” complexes will be inactive during “peace time”.
Potential drawback of having melanin production is mostly mitigated through periplasmic confinement.
800-1500 Gy can be easily shrugged off by vegetative Little Boys. Above 1500 triggers emergency endospore formation/release (see above)
Biofilm Formation:
Little Boys will actively form biofilms, both inside hosts and in environments, using their plastic shells (they are supposed to be the only ones to metabolize UHMWPE) to stick together, to concentrate themselves closer the richer parts of substrate, and to shield themselves from any outside influence (caveat - the organism is non-motile outside the biofilm complex). Colonies are complex, and create a microclimate of its own. Structure of biofilm protects the Little Boys that directly contact the substrate from harm, and thus allows for more aggressive substrate assimilation unimpeded by any unfriendly influence.
A dedicated signaling compound accumulates in colonial boys, forcing the “topmost” bacteria to “flake off” from the colony, form endospores and float in vast numbers to new horizons.
In vivo this will cause rapid blood-borne propagation, with eventual compromise of respiratory system ( yay bacterial metastases!
yay airborne plague!
).
Environment compatibility:
what we know about the environment is more than sufficient to make Little Boy capable of consuming LII biololymers with significant redundancy (additional enzymes for handling unusual metabolic inputs, just if some silly LII life tries to escape by using, say, rare optic isomers...)
The niche
"parasite/facultative decomposer" (you read it right, facultative decomposer). After all, Little Boy is designed to shut down whole ecosystems, not form new ones.
Additional redundancy:
Ribozymes used where possible to complicate reverse-engineering, increase metabolism speed and decrease genome size
Main metabolic pathways are at least double redundant. Every component of backup of a critical pathway is significantly mutable, to ensure quick formation of resistance to possible attempts at antibiotic treatment.
Active antibiotic resistance (AAR) systems built-in by default (xenometabolite detection and efflux, xenometabolite inactivation, etc), at least two additional, redundant highly mutable AAR systems present.
Several external digestive enzymes that are aggression factors against host are highly mutable, to improve probability of hostile antibody counteraction and destruction.
Metavariation systems (constructs that rapidly increase mutation rates in response to stress and environment change associated with destruction of adjacent Little Boy cells) to increase mutation when a colony is threatened.
Distributed genome, >40% of genotype is encoded extra-chromosomaly (stringent conjunctive plasmids, etc) to increase mobility (see below), improve DNA protection in endospores and complicate reverse-engineering
Several methods for exchanging extra-chromosomal genetic material between strains of little boys (relatively secure against potential viral abuse).
Free bonuses
- Airborne dispersal bonus:
basically, as soon as a Lamprey gets a colony of Little Boys in its respiratory tract, Little Boy gets airborne. And because every single Little Boy bacterium is tough as hell, every tiny slime drop gets formidably contagious.
- endosporal bonus:
Even if the phagocytes in the host are super-persistent and chemically aggressive, the endospore will linger in the hostile cell until the host cell dies, assuming that side products of enzymes that were tearing down the UHMWPE cell wall during endospore release did not unmake host cell outright. After the host cell’s death the Little Boy shall resume its destructive activities. The hypothetical super-phagocyte will thus serve to distribute infection throughout organism of the victim, forming bacterial metastases.
- UHMWPE bonus:
UHMWPE-metabolic pathways can be (AND SHOULD BE) used to attack several similar classes of industrial polymers (HMWPE, UHMWPE), thus granting the Little Boy ability to score additional damage against infrastructure, and even potentially compromise bio-containment protocols by actively attacking air filtration systems and polymer barriers.
Any ecological niche that is colonized by LB will be inhospitable for normal life for years to come (toxic metabolism)
- Antibody-philiac:
Apparently, surface proteins will attract antibodies. However, those will not be able to severely harm a creature with a UHMWPE cell wall. Thus, antibody-rich environment will amount to a protein soup the Little Boy will proceed to break down and consume.
- Burned-until-it-was-clean bonus:
Burning down the infected swaths of biosphere not only fails to kill of the pathogen, but causes airborne dispersal of endospores stuck to the soot particulate, thus facilitating ecosystem-wide contamination.
- Sadistic bonus:
Hosts will die a very torturous death. *cold robotic stare* *snicker*
Problems
- Catabolism of UHMWPE (normal part or re-building a cell wall) will have wastes that are toxic to "normal" life. Hosts will have their blood vessels scorched by substances that are essentially hazardous paint thinners. Asymptomatic course exceeding one week is theoretically possible, but not guaranteed.
- Problems with "locking in" the virulence down-selection (actually a non-issue, as it will arise AFTER most complex life is converted to plastic. Still, an engineering trade-off)
- Slow (relatively low rate of reproduction)
it will spread slowly, but steadily. Thus, can be contained early on, if in small dryland isolates (containing it in a marine environment is not a realistic possibility, however).
Bear in mind that after a critical mass is reached, and/or a major water body is contaminated, its game over for Lampreys.
- non-motile outside biofilm
), we can most certainly create organisms that biosynthesize ultra high molecular weight polyethylene (metabolizing it will be a tiny bit more complicated, but many strains of Pseudomonas stutzeri can handle HMWPE, so fine-tuning the enzyme complexes that are well studied and stored in the onboard database to handle UHMWPE is a pretty much manageable issue)
