Related Experiment Video

Updated: Jun 4, 2026

Metal-Limited Growth of Neisseria gonorrhoeae for Characterization of Metal-Responsive Genes and Metal Acquisition from Host Ligands
07:26

Metal-Limited Growth of Neisseria gonorrhoeae for Characterization of Metal-Responsive Genes and Metal Acquisition from Host Ligands

Published on: March 4, 2020

Interplay between manganese and zinc homeostasis in the human pathogen Streptococcus pneumoniae

Faith E Jacobsen1, Krystyna M Kazmierczak, John P Lisher

  • 1Department of Chemistry, Indiana University, Bloomington, IN 47405-7102, USA.

Metallomics : Integrated Biometal Science
|January 29, 2011
PubMed

Insights

Zinc toxicity in Streptococcus pneumoniae causes manganese deficiency, hindering growth. Restoring manganese levels fully reverses this effect, suggesting competition for uptake.

Area of Science:

  • Microbiology
  • Biochemistry
  • Molecular Biology

Background:

  • Streptococcus pneumoniae requires metal ions for growth.
  • Metal ion homeostasis is crucial for bacterial survival and virulence.
  • Understanding metal ion interactions is key to developing new antimicrobial strategies.

Purpose of the Study:

  • To investigate the impact of zinc (Zn(II)) stress on manganese (Mn(II)) homeostasis in Streptococcus pneumoniae.
  • To elucidate the mechanisms underlying zinc-induced growth defects.
  • To identify genes and pathways affected by zinc stress.

Main Methods:

  • Inductively Coupled Plasma-Mass Spectrometry (ICP-MS) for metal ion quantification.
  • Growth curve analysis to assess phenotypes.
  • DNA microarray analysis for transcriptional profiling.

Main Results:

  • High cell-associated Mn(II) in Streptococcus pneumoniae, comparable to Zn(II).
  • Zn(II) stress (100–200 microM) induced a slow-growth phenotype and reduced total Mn(II) levels.
  • Supplementation with 10 microM Mn(II) fully restored growth and Mn(II) levels.
  • Zinc stress upregulated czcD (zinc effluxer) and genes involved in nitric oxide detoxification (nmlR) and Mn(II) uptake (psaBCA).

Conclusions:

  • Zn(II) toxicity leads to cytoplasmic Mn(II) deficiency in Streptococcus pneumoniae.
  • Competition at the Mn(II) uptake transporter PsaA is a likely cause of Mn(II) deficiency.
  • Zinc stress triggers a pleiotropic transcriptional response, including cell wall stress and NO detoxification pathways.

More Related Videos

Using Mycobacterium smegmatis as a Bioindicator for Zinc-Limited Growth Conditions in Mycobacteria08:24

Using Mycobacterium smegmatis as a Bioindicator for Zinc-Limited Growth Conditions in Mycobacteria

Published on: September 20, 2024

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness12:21

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness

Published on: September 28, 2022

Related Concept Videos

Microbes and Other Elemental Cycles01:24

Microbes and Other Elemental Cycles

Microbial activity plays a pivotal role in the biogeochemical cycling of iron and manganese, especially at the redox gradients characteristic of stratified aquatic environments. These cycles are driven by microbial transformations between oxidized and reduced forms of the metals, allowing organisms to exploit them for metabolic energy and structural purposes.Iron Cycling Across Redox GradientsIn neutral, oxygen-rich surface waters, iron is predominantly found in its oxidized, insoluble ferric...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
Malaria01:29

Malaria

Malaria pathogenesis in humans reflects a delicate interplay between parasite biology and host response. Clinical illness reflects a host’s immune response to the parasite’s asexual replication cycle, which is often asymptomatic in individuals with partial immunity. From the parasite's perspective, transmission between mosquito and human with minimal host pathology is evolutionarily advantageous. Among the six Plasmodium species infecting humans, P. falciparum and P. vivax dominate in global...
Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps: