Cellular Memory of HipA-Induced Growth Arrest: The Length of Cell Growth Arrest Becomes Shorter for Each Successive Induction

Toxin–antitoxin (TA) systems are genetic modules found commonly in bacterial genomes. HipA is a toxin protein encoded from the <i>hipBA</i> TA system in the genome of <i>Escherichia coli.</i> Ectopic expression of <i>hipA</i> induces cell growth arrest. Unlike the...

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Main Authors: Chun-Yi Lin, Sanya Hatimi, Peter Robert Tupa, Hisako Masuda
Format: Article
Language:English
Published: MDPI AG 2021-12-01
Series:Microorganisms
Subjects:
Online Access:https://www.mdpi.com/2076-2607/9/12/2594
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author Chun-Yi Lin
Sanya Hatimi
Peter Robert Tupa
Hisako Masuda
author_facet Chun-Yi Lin
Sanya Hatimi
Peter Robert Tupa
Hisako Masuda
author_sort Chun-Yi Lin
collection DOAJ
description Toxin–antitoxin (TA) systems are genetic modules found commonly in bacterial genomes. HipA is a toxin protein encoded from the <i>hipBA</i> TA system in the genome of <i>Escherichia coli.</i> Ectopic expression of <i>hipA</i> induces cell growth arrest. Unlike the cell growth arrest caused by other TA toxins, cells resume growth from the HipA-induced cell growth arrest phase after a defined period of time. In this article, we describe the change in the length of growth arrest while cells undergo repeated cycles of <i>hipA</i> induction, growth arrest and regrowth phases. In the multiple conditions tested, we observed that the length of growth arrest became successively shorter for each round of induction. We verified that this was not due to the appearance of HipA-resistant mutants. Additionally, we identified conditions, such as the growth phase of the starting culture and growth vessels, that alter the length of growth arrest. Our results showed that the length of HipA-induced growth arrest was dependent on environmental factors—in particular, the past growth environment of cells, such as a previous <i>hipA</i> induction. These effects lasted even after multiple rounds of cell divisions, indicating the presence of cellular “memory” that impacts cells’ response to HipA-induced toxicity.
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spelling doaj.art-6441ba67dc794752bef98416170643012023-11-23T09:40:21ZengMDPI AGMicroorganisms2076-26072021-12-01912259410.3390/microorganisms9122594Cellular Memory of HipA-Induced Growth Arrest: The Length of Cell Growth Arrest Becomes Shorter for Each Successive InductionChun-Yi Lin0Sanya Hatimi1Peter Robert Tupa2Hisako Masuda3Department of Biochemistry and Molecular Biology, Rutgers University, 675 Hoes Lane, Piscataway, NJ 08854, USASchool of Sciences, Indiana University Kokomo, 2300 S Washington St., Kokomo, IN 46902, USASchool of Sciences, Indiana University Kokomo, 2300 S Washington St., Kokomo, IN 46902, USADepartment of Biochemistry and Molecular Biology, Rutgers University, 675 Hoes Lane, Piscataway, NJ 08854, USAToxin–antitoxin (TA) systems are genetic modules found commonly in bacterial genomes. HipA is a toxin protein encoded from the <i>hipBA</i> TA system in the genome of <i>Escherichia coli.</i> Ectopic expression of <i>hipA</i> induces cell growth arrest. Unlike the cell growth arrest caused by other TA toxins, cells resume growth from the HipA-induced cell growth arrest phase after a defined period of time. In this article, we describe the change in the length of growth arrest while cells undergo repeated cycles of <i>hipA</i> induction, growth arrest and regrowth phases. In the multiple conditions tested, we observed that the length of growth arrest became successively shorter for each round of induction. We verified that this was not due to the appearance of HipA-resistant mutants. Additionally, we identified conditions, such as the growth phase of the starting culture and growth vessels, that alter the length of growth arrest. Our results showed that the length of HipA-induced growth arrest was dependent on environmental factors—in particular, the past growth environment of cells, such as a previous <i>hipA</i> induction. These effects lasted even after multiple rounds of cell divisions, indicating the presence of cellular “memory” that impacts cells’ response to HipA-induced toxicity.https://www.mdpi.com/2076-2607/9/12/2594HipAtoxin–antitoxin systempersistergrowth arrestcellular memory
spellingShingle Chun-Yi Lin
Sanya Hatimi
Peter Robert Tupa
Hisako Masuda
Cellular Memory of HipA-Induced Growth Arrest: The Length of Cell Growth Arrest Becomes Shorter for Each Successive Induction
Microorganisms
HipA
toxin–antitoxin system
persister
growth arrest
cellular memory
title Cellular Memory of HipA-Induced Growth Arrest: The Length of Cell Growth Arrest Becomes Shorter for Each Successive Induction
title_full Cellular Memory of HipA-Induced Growth Arrest: The Length of Cell Growth Arrest Becomes Shorter for Each Successive Induction
title_fullStr Cellular Memory of HipA-Induced Growth Arrest: The Length of Cell Growth Arrest Becomes Shorter for Each Successive Induction
title_full_unstemmed Cellular Memory of HipA-Induced Growth Arrest: The Length of Cell Growth Arrest Becomes Shorter for Each Successive Induction
title_short Cellular Memory of HipA-Induced Growth Arrest: The Length of Cell Growth Arrest Becomes Shorter for Each Successive Induction
title_sort cellular memory of hipa induced growth arrest the length of cell growth arrest becomes shorter for each successive induction
topic HipA
toxin–antitoxin system
persister
growth arrest
cellular memory
url https://www.mdpi.com/2076-2607/9/12/2594
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AT peterroberttupa cellularmemoryofhipainducedgrowtharrestthelengthofcellgrowtharrestbecomesshorterforeachsuccessiveinduction
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