Lec 1 Protection against phages and Archaeal Viruses Flashcards
Archaea are very different from Bacteria
NOT Virus
Archaea are very different from Bacteria:
different phospholipids in their membranes
different cell wall structures (most have protein S-layers, no peptidoglycan but some (very few) have pseudopeptidoglycan aka pseudomurein)
Pseudopeptidoglycan is not targetted by stuff like streptomycin
promoters for transcription (and RNA polymerase) more similar to eukaryotes. There are more than 2 archaeal lineages.
many isolated ones are extremophiles, many known only from sequences.
Archaea Viruses General
Very different physiology (claws at the tips, irregular capsid shape)
First isolates from Euryarchaeota were like tailed phages. Subsequent research has shown that most archaeal viruses are completely different from bacteriophages
Just 1 ssDNA archaea virus all other archaeal viruses have dsDNA genomes, No RNA viruses (not isolated but possibly discovered by metagenomics?)
some have CIRCULAR dsDNA packed in the virion, which have NEVER BEEN FOUND IN BACTERIOPHAGES, found in the virion only.
AFV-1, Acidianus filamentous virus 1
Archaea virus example
AFV-1, Acidianus filamentous virus 1
hook structures at the ends of the virions
Uses them to grab onto the cell’s pilus, enters host w/ pili contraction
Why are there so many “UNUSUAL” SHAPES in the archaeal viruses?
eg. STIV and 4 adaptations
Viruses from the extreme environments have adaptations that make the particles able to withstand the high temperatures and low pH
STIV, Sulfolobus turreted icosahedral virus:
- TIGHTLY PACKED SUBUNIT structure
- HIGH PROLINE content
- INCREASE IN ELECTROSTATIC INTERACTIONS in the CAPSID PROTEINS
- increased POLAR SURFACE AREA
Archaeal viruses life strategies
Many can be TEMPERATE (enter lysogenic state)
Many have ENVELOPES, whereas this is VERY RARE IN BACTERIOPHAGES
Many are RELEASED from CELLS WITHOUT LYSIS.
Mechanism is unclear. Exocytosis? Levers?
Restriction Modification Systems and Viral adaptation
Restriction Modification Systems
Could be involved in PLASMID MAINTENANCE
Many phages eg. T4 modify their DNA so they are impermeable to it, such as inactivating restriction systems (T7)
Type I 3 components – methylation, recognition,
restriction (cleavage). Work together.
Cleavage is NOT SITE SPECIFIC. Eg. E. coli K1 system
Type II Most useful in CLONING. SITE SPECIFIC.
Separate Methylase and Cleavage Enzyme.
Type 2S cleaves off target
Type IV Attack METHYLATED DNA.
Abortive infection systems
2 examples
Abortive infection systems have
Infected cell commits suicide or
blocks growth to prevent phage replication
Eg. 1. RexAB system in E. coli Lambda
lysogens. (Already mentioned as example of
Lysogenic conversion)
2.ToxIN system of Erwinia carotovora
(now Pectobacterium atrosepticum), AbiQ
in Lactic bacteria, etc.
ToxN is the growth INHIBITOR, produced CONSTITUTIVELY
ToxI is the ANTITOXIN, negates ToxN, as long as ToxI is produced (the cell fells its not invaded). Usually unstable wrt ToxN.
rexAB genes expressed by strains LYSOGENIC for LAMBDA! The virus must repress them or else.
ToxI can be made/mimicked/stabilized by virus, or ToxN can be inhibited
CRISPRS and Defence
CRISPRs - clustered regularly interspaced short
palindromic repeats
Found in 40-50 % of Bacterial and 90 % of
Archaeal genomes.
Function in association with CAS (CRISPR -associated proteins) to kill foreign DNA (and RNA)
Not too many RNA systems. Read the notes!