Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pulmonary Tuberculosis II01:28

Pulmonary Tuberculosis II

1.0K
Tuberculosis, or TB, is a bacterial infectious disease caused by Mycobacterium tuberculosis. While its primary impact is on the lungs, leading to pulmonary tuberculosis, it can also affect various other organs, a condition referred to as extrapulmonary tuberculosis.
Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
1.0K
Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

2.4K
The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
2.4K
Viral Replication: Lysogenic Cycle01:16

Viral Replication: Lysogenic Cycle

997
The lysogenic cycle is a crucial viral replication strategy that allows bacteriophages to persist within host cells without immediately destroying them. This process is primarily observed in temperate phages, such as bacteriophage lambda (λ), which infects Escherichia coli. The cycle allows the viral genome to persist across bacterial generations while keeping host cells viable.Integration of the Viral GenomeUpon infection, bacteriophage lambda attaches to the bacterial surface and injects...
997
Stringent Response in E. coli01:23

Stringent Response in E. coli

190
Bacterial growth is closely tied to nutrient availability, with cells proliferating exponentially under favorable conditions and entering a stationary phase when resources become scarce. This transition is mediated by a regulatory mechanism known as the stringent response, which allows bacteria to adapt to nutrient deprivation by modulating gene expression and metabolic activity.During nutrient scarcity, intracellular amino acid levels decline. It results in the accumulation of uncharged tRNAs...
190
Lysogenic Cycle of Bacteriophages00:43

Lysogenic Cycle of Bacteriophages

66.8K
In contrast to the lytic cycle, phages infecting bacteria via the lysogenic cycle do not immediately kill their host cell. Instead, they combine their genome with the host genome, allowing the bacteria to replicate the phage DNA along with the bacterial genome. The incorporated copy of the phage genome is called the prophage. Some prophages can re-activate and enter the lytic cycle. This often occurs in response to a perturbation, such as DNA damage, but can also transpire in the absence of...
66.8K
Pulmonary Tuberculosis I01:29

Pulmonary Tuberculosis I

579
Tuberculosis, often called TB, is a contagious illness primarily caused by Mycobacterium tuberculosis. It mainly affects the lung parenchyma but can also impact other body parts.
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
Mode of...
579

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Cryo-EM structure of the <i>Mycobacterium smegmatis</i> MmpL5-AcpM complex.

mBio·2024
Same author

Structures of the mycobacterial MmpL4 and MmpL5 transporters provide insights into their role in siderophore export and iron acquisition.

PLoS biology·2024
Same author

Structural modeling and characterization of the Mycobacterium tuberculosis MmpL3 C-terminal domain.

FEBS letters·2024
Same author

M. tuberculosis AlkX Encoded by <i>rv3249c</i> Regulates a Conserved Alkane Hydroxylase System That Is Important for Replication in Macrophages and Biofilm Formation.

Microbiology spectrum·2022
Same author

Complete Characterization of Polyacyltrehaloses from <i>Mycobacterium tuberculosis</i> H37Rv Biofilm Cultures by Multiple-Stage Linear Ion-Trap Mass Spectrometry Reveals a New Tetraacyltrehalose Family.

Biochemistry·2021
Same author

Identification of residues important for M. tuberculosis MmpL11 function reveals that function is modulated by phosphorylation in the C-terminal domain.

Molecular microbiology·2020

Related Experiment Video

Updated: Dec 6, 2025

Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1
07:42

Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1

Published on: February 28, 2025

783

Modulation of the M. tuberculosis cell envelope between replicating and non-replicating persistent bacteria.

Haley Stokas1, Heather L Rhodes1, Georgiana E Purdy1

  • 1Oregon Health & Science University, Department of Molecular Microbiology & Immunology, Portland, OR, 97239, United States.

Tuberculosis (Edinburgh, Scotland)
|October 9, 2020
PubMed
Summary

Mycobacterium tuberculosis persists in hosts by entering a non-replicating persistence (NRP) state, involving cell envelope changes. Serine/threonine protein kinases (STPKs) may mediate these adaptations.

Keywords:
DormancyLipidsMycobacterium tuberculosisMycolic acids

More Related Videos

Preparation of Mycobacterium Tuberculosis Culture Filtrate to Understand TB Pathogenesis
07:32

Preparation of Mycobacterium Tuberculosis Culture Filtrate to Understand TB Pathogenesis

Published on: March 28, 2025

832
Growth of Mycobacterium tuberculosis Biofilms
09:03

Growth of Mycobacterium tuberculosis Biofilms

Published on: February 15, 2012

24.3K

Related Experiment Videos

Last Updated: Dec 6, 2025

Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1
07:42

Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1

Published on: February 28, 2025

783
Preparation of Mycobacterium Tuberculosis Culture Filtrate to Understand TB Pathogenesis
07:32

Preparation of Mycobacterium Tuberculosis Culture Filtrate to Understand TB Pathogenesis

Published on: March 28, 2025

832
Growth of Mycobacterium tuberculosis Biofilms
09:03

Growth of Mycobacterium tuberculosis Biofilms

Published on: February 15, 2012

24.3K

Area of Science:

  • Microbiology
  • Pathogenesis
  • Bacterial Physiology

Background:

  • Mycobacterium tuberculosis (M. tuberculosis) is a successful human pathogen.
  • Pathogen survival relies on persistence in nutrient-poor, low-oxygen host environments.
  • This persistence involves a transition from replication to a non-replicating persistence (NRP) state.

Purpose of the Study:

  • To review cell envelope alterations in M. tuberculosis during the transition to NRP.
  • To explore the role of serine/threonine protein kinases (STPKs) in mediating these changes.

Main Methods:

  • Review of in vitro studies on M. tuberculosis NRP.
  • Analysis of patient and animal model data for NRP phenotypes.
  • Focus on cell envelope composition and structure differences.
  • Examination of STPK involvement in regulating NRP.

Main Results:

  • NRP M. tuberculosis exhibits distinct cell envelope characteristics compared to replicating forms.
  • Environmental cues like low oxygen and nutrient scarcity trigger the NRP shift.
  • STPKs are implicated as key regulators of metabolic and structural changes during NRP.

Conclusions:

  • Cell envelope remodeling is crucial for M. tuberculosis persistence.
  • STPKs are potential mediators of adaptation to host-imposed stresses.
  • Understanding these mechanisms can inform novel therapeutic strategies against M. tuberculosis.