science

TisB-IstR toxin-antitoxin system

TisB-IstR toxin-antitoxin system is a science topic covered in the lgStudy science library. This page brings together a partial reference excerpt, illustrations, worked examples, real-world applications and a short study plan, so you can understand TisB-IstR toxin-antitoxin system rather than just read about it. In short: The TisB-IstR toxin-antitoxin system is the first known toxin-antitoxin system which is induced by the SOS response in response to DNA damage. IstR-1 and IstR-2 IstR sRNA (inhibitor of SOS-induced toxicity by RNA) is a family of non-coding RNA first identified in Escherichia coli.

Key takeaways

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Reference excerpt

The TisB-IstR toxin-antitoxin system is the first known toxin-antitoxin system which is induced by the SOS response in response to DNA damage.

IstR-1 and IstR-2 IstR sRNA (inhibitor of SOS-induced toxicity by RNA) is a family of non-coding RNA first identified in Escherichia coli. There are two small RNAs encoded by the IstR locus: IstR-1 and IstR-2, of which IstR-1 works as antitoxins against the toxic protein TisB (toxicity-induced by SOS B) which is encoded by the neighbouring tisAB gene. IstR-1 is a 75 nucleotide transcript expressed constitutively throughout growth, whereas IstR-2 is a 140 nucleotide transcript induced by Mitomycin C (MMC). Both IstR-2 and tisAB are thought to be regulated by LexA while IstR-1 is constitutively transcribed. Deletion analysis confirmed the function of IstR, E. coli strain K-12 could not grow in the absence of IstR when tisAB was present. Inserting IstR genes on a plasmid allowed the bacteria to grow normally. Further studies showed that expression of IstR-1 alone is enough to remedy the toxic effects of TisB. IstR-2 is not involved in the regulation of tisAB.

TisAB The tisAB locus codes for two genes: tisA and tisB. The tisA reading frame was shown through a translation assay to not be translated. Its sequence is unconserved across species. TisB is a 29 amino acid peptide widely conserved in enterobacteria. TisB is responsible for conferring toxicity through suspected membrane disruption. Upon transcription of the tisB gene, a +1 inactive primary transcript mRNA is produced, which must be endonucleolytically processed 42 nucleotides from the 5' end to yield a +42 translationally competent mRNA. In the +42 form, the mRNA has a ribosome loading/standby site in an unstructured region >80 nt upstream of the tisB ribosome binding site, thus allowing translation of the TisB protein. This standby site is structurally unavailable in the inactive forms of the tisB mRNA (the +1 form and the +106 form produced by RNase III cleavage).

Mechanism of TisB inhibition by IstR-1

IstR-1 is thought to both inhibit translation of the TisB toxin, and promote RNase III cleavage of the RNA duplex formed when IstR-1 base pairs to tisB mRNA. Binding of the complementary sequence of istR-1 sRNA to tisB mRNA in the ribosome standby site is thought to prevent loading of ribosomes and therefore prevent translation of the TisB protein. A RACE analysis confirmed that IstR-1 binds TisB mRNA and the duplex is then degraded by RNase III. Degradation results in a +106 form, an inactive 249 nt transcript which cannot be translated.

Proposed function of the IstR-TisB toxin-antitoxin system The proposed function of this toxin-antitoxin system is to cause growth arrest, rather than cell death, in response to DNA damage, allowing time for repair processes to occur. TisB translation is under LexA control, so it is induced by DNA damage as part of the SOS response. Under normal conditions, very little tisB mRNA is synthesised and translation is inhibited, but when DNA damage occurs tisAB is strongly induced causing overexpression, which overrides inhibition by depleting the IstR-1 pool. Experimental data has shown effects of TisB to be decreases in transcription, translation and replication, RNA degradation and ribosome disassembly. TisB does not affect transcription and translation directly in vitro, so these effects are thought to be downstream consequences of membrane damage. TisB insertion into the membrane is thought to result in a loss of membrane potential. This could account for a decrease in ATP concentration in cells following triggering of the SOS response, causing slowing of cellular processes and inhibited cell growth. Also, it has been suggested that TisB may have a role in stabilising the bacterial persistence state after treatment of Escherichia coli with fluoroquinolones.

See also Toxin-antitoxin system Sib RNA hok/sok system

References

Illustrations

Worked examples

Example 1 — a first encounter with TisB-IstR toxin-antitoxin system

Start with the simplest possible case. Write down what TisB-IstR toxin-antitoxin system claims or describes in one sentence, then invent the smallest concrete situation in which that sentence is true. In science, the smallest case is usually a single object, a single equation or a single measurement. Check that every symbol or term in your sentence has a meaning in that case.

Example 2 — changing one variable

Take the situation from Example 1 and change exactly one quantity: double it, halve it, or set it to zero. Predict what should happen to TisB-IstR toxin-antitoxin system before you calculate. Comparing your prediction with the result is the fastest way to find out whether you understand the idea or only the words.

Example 3 — an exam-style question

Typical questions about TisB-IstR toxin-antitoxin system ask you to (a) state it precisely, (b) apply it to given data, and (c) explain a limitation. Practise writing all three answers in under five minutes; the third part is what separates a full-mark answer from an average one.

Applications of TisB-IstR toxin-antitoxin system

In research: TisB-IstR toxin-antitoxin system appears in science research whenever the underlying quantities have to be modelled precisely. Papers usually cite it as a starting assumption and then explore where it breaks down.
In technology and industry: Engineering practice reuses TisB-IstR toxin-antitoxin system in design rules, simulations and safety margins. Knowing the idea lets you read a specification sheet and understand why the numbers look the way they do.
In the classroom: TisB-IstR toxin-antitoxin system is common in secondary-school and first-year university syllabi. It links to neighbouring topics Antisense RNA, RNA antitoxins, Toxins, so understanding it makes those chapters shorter.
In everyday life: Look for TisB-IstR toxin-antitoxin system outside the textbook — in sport, cooking, traffic, electronics or the sky above you. An example you found yourself is remembered far longer than one you were given.

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How to study TisB-IstR toxin-antitoxin system in 20 minutes

Read the reference excerpt below once, without taking notes.
Close the page and write down what TisB-IstR toxin-antitoxin system means in your own words.
Compare your version with the excerpt and mark what you missed.
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Frequently asked questions

What is TisB-IstR toxin-antitoxin system in simple terms?

The TisB-IstR toxin-antitoxin system is the first known toxin-antitoxin system which is induced by the SOS response in response to DNA damage. IstR-1 and IstR-2 IstR sRNA (inhibitor of SOS-induced toxicity by RNA) is a family of non-coding RNA first identified in Escherichia coli.

Why does TisB-IstR toxin-antitoxin system matter?

Because it connects several science ideas at once: it gives you a definition you can apply, a quantity you can calculate, and a way to check whether a result is plausible.

How should I study TisB-IstR toxin-antitoxin system?

Read the excerpt, restate it from memory, then work through the examples and applications listed on this page. The five-step study plan above takes about twenty minutes.

What does this page cover?

It gives you a compact reference excerpt plus original lgStudy explanations, examples, applications and study material on TisB-IstR toxin-antitoxin system.