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== Background Information==

- addition modules have two genes: toxin genes and an antitoxin genes

- modules mediate plasmid maintenance by killing plasmid free cells via what you call, post segregational killing.

- Operons are autoregulated at transcriptional level to control toxin/antitoxin modules

- Maintenance prevents the lethal effect of the toxin.

- There have been two structures that are found, that have similar 3D structure

- 1. Kid from E.coli in plasmid R1

- 2. CcdB from E.coli in plasmid F.

- modules found so far such as ChpA/MazEF and ChpB, which are homologous genes to the addiction modules, are involved in cell death that is thought to be triggered by antibiotics.

- operons encode stable toxin and their antidote

- opersons play an important role in plasmid partitioning and cellular response to stress.

- Family of toxins (MazF/ChpAK/PemK) encodes endoribonuclease that activates cellular mRNAs by cleaving them at specific sites

- This study, there is a B.subtilis gene encode a member of RNases that they call Endo A.

- A coexpression of an upstream gene (YdcD) reverses toxin.

- YdcD inhibits EndoA activity.

- endoA has similar cleavage patterns specificity to MazF/PemK, with cleavage produces with a 3’P and 5’OH group.

- This is the first example of an antitoxin-toxin system of B. subtilis.

- bacteria rely on addiction modules to maintain plasmids within populations.

- These modules consist of operon where one cistron encodes a stable toxin and is preceded by an encoding unstable antitoxin.

- Cells that do not inherit the plasmid encoded operon will not produce antitoxin and inhibited by the toxin via post segregational killing.

- So once this operon is expressed, the bacterial strain is addicted to the antitoxin for survival.

- It is known that genomes of most bacteria has a toxin-antitoxin TA loci.

- These loci have been shown to be induced by stressful conditions.

- It has been shown that antitoxin can also inhibit its own expression by binding to its own promoter region with complexed toxin as corepressor.

-

==Structure==

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@@ Line 2: / Line 2: @@
 == Background Information==
+- addition modules have two genes: toxin genes and an antitoxin genes
+-	modules mediate plasmid maintenance by killing plasmid free cells via what you call, post segregational killing.
+-	Operons are autoregulated at transcriptional level to control toxin/antitoxin modules
+-	Maintenance prevents the lethal effect of the toxin.
+-	There have been two structures that are found, that have similar 3D structure
+-	1. Kid from E.coli in plasmid R1
+-	2. CcdB from E.coli in plasmid F.
+-	modules found so far such as ChpA/MazEF and ChpB, which are homologous genes to the addiction modules, are involved in cell death that is thought to be triggered by antibiotics.
+-	operons encode stable toxin and their antidote
+-	opersons play an important role in plasmid partitioning and cellular response to stress.
+-	Family of toxins (MazF/ChpAK/PemK) encodes endoribonuclease that activates cellular mRNAs by cleaving them at specific sites
+-	This study, there is a B.subtilis gene encode a member of RNases that they call Endo A.
+-	A coexpression of an upstream gene (YdcD) reverses toxin.
+-	YdcD inhibits EndoA activity.
+-	endoA has similar cleavage patterns specificity to MazF/PemK, with cleavage produces with a 3’P and 5’OH group.
+-	This is the first example of an antitoxin-toxin system of B. subtilis.
+-	bacteria rely on addiction modules to maintain plasmids within populations.
+-	These modules consist of operon where one cistron encodes a stable toxin and is preceded by an encoding unstable antitoxin.
+-	Cells that do not inherit the plasmid encoded operon will not produce antitoxin and inhibited by the toxin via post segregational killing.
+-	So once this operon is expressed, the bacterial strain is addicted to the antitoxin for survival.
+-	It is known that genomes of most bacteria has a toxin-antitoxin TA loci.
+-	These loci have been shown to be induced by stressful conditions.
+-	It has been shown that antitoxin can also inhibit its own expression by binding to its own promoter region with complexed toxin as corepressor.
+-
 ==Structure==