MinC Mutants Deficient in MinD- and DicB-Mediated Cell Division Inhibition Due to Loss of Interaction with MinD, DicB, or a Septal Component

Zhou, Huaijin; Lutkenhaus, Joe

doi:10.1128/jb.187.8.2846-2857.2005

Cited by 61 publications

(82 citation statements)

References 42 publications

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“…The second mechanism is the result of a decreased expression of minDE and divIVA, which are involved in spatially correct septum placement. The MinCD complex negatively regulates formation of the cytokinetic Z-ring to midcell by preventing its formation near the poles (Zhou & Lutkenhaus, 2005). Another strategy of L. monocytogenes to suppress cell division might be to decrease expression of fteX and ftsE.…”

Section: Discussionmentioning

confidence: 99%

The heat-shock response of Listeria monocytogenes comprises genes involved in heat shock, cell division, cell wall synthesis, and the SOS response

et al. 2007

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The food-borne pathogen Listeria monocytogenes has the ability to survive extreme environmental conditions due to an extensive interacting network of stress responses. It is able to grow and survive at relatively high temperatures in comparison with other non-sporulating food-borne pathogens. To investigate the heat-shock response of L. monocytogenes, whole-genome expression profiles of cells that were grown at 37 6C and exposed to 48 6C were examined using DNA microarrays. Transcription levels were measured over a 40 min period after exposure of the culture to 48 6C and compared with those of unexposed cultures at 37 6C. After 3 min, 25 % of all genes were differentially expressed, while after 40 min only 2 % of all genes showed differential expression, indicative of the transient nature of the heat-shock response. The global transcriptional response was validated by analysing the expression of a set of 13 genes by quantitative PCR. Genes previously identified as part of the class I and class III heat-shock response and the class II stress response showed induction at one or more of the time points investigated. This is believed to be the first study to report that several heat-shock-induced genes are part of the SOS response in L. monocytogenes. Furthermore, numerous differentially expressed genes that have roles in the cell division machinery or cell wall synthesis were down-regulated. This expression pattern is in line with the observation that heat shock results in cell elongation and prevention of cell division.

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Section: Discussionmentioning

confidence: 99%

The heat-shock response of Listeria monocytogenes comprises genes involved in heat shock, cell division, cell wall synthesis, and the SOS response

et al. 2007

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“…Plasmids pSEB104CD (P BAD ::minC minD), pSEB104CDE (P BAD ::minC minD minE), and pJB216E (P lac ::minE) were described previously (21). The minE D45A and minE D45A/V49A mutations were introduced into pSEB104CDE and pJB216E using the QuikChange II kit according to the manufacturer's instructions (Agilent Technologies).…”

Section: Methodsmentioning

confidence: 99%

“…In the presence of 0.2% arabinose JS964/ pSEB104CDE grew well and exhibited a WT morphology. Under these conditions the Min proteins are expressed near the physiological level (21). In contrast, JS964 containing pSEB104CDE-D45A/V49A or pSEB104CDE-D45A displayed poor colony formation in the presence of arabinose (Fig.…”

Section: D45a/v49mentioning

confidence: 99%

“…The latent conformation is a 6β-stranded structure that diffuses in the cytoplasm because the segments of MinE that interact with MinD (β1 strand at the dimer interface) and the membrane (N-terminal amphipathic helices also called membrane targeting sequences, MTS) are masked. In contrast, the active conformation consists of a 4β-stranded structure with the MTS bound to the membrane and the released β1 strand and part of the loop region (residues [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28] converted to an alpha helix bound to MinD (Fig. 1).…”

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confidence: 99%

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MinE conformational dynamics regulate membrane binding, MinD interaction, and Min oscillation

Park

Villar

Artigues

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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In Escherichia coli MinE induces MinC/MinD to oscillate between the ends of the cell, contributing to the precise placement of the Z ring at midcell. To do this, MinE undergoes a remarkable conformational change from a latent 6β-stranded form that diffuses in the cytoplasm to an active 4β-stranded form bound to the membrane and MinD. How this conformational switch occurs is not known. Here, using hydrogen-deuterium exchange coupled to mass spectrometry (HDX-MS) we rule out a model in which the two forms are in rapid equilibrium. Furthermore, HDX-MS revealed that a MinE mutant (D45A/V49A), previously shown to produce an aberrant oscillation and unable to assemble a MinE ring, is more rigid than WT MinE. This mutant has a defect in interaction with MinD, suggesting it has difficulty in switching to the active form. Analysis of intragenic suppressors of this mutant suggests it has difficulty in releasing the N-terminal membrane targeting sequences (MTS). These results indicate that the dynamic association of the MTS with the β-sheet is fine-tuned to balance MinE's need to sense MinD on the membrane with its need to diffuse in the cytoplasm, both of which are necessary for the oscillation. The results lead to models for MinE activation and MinE ring formation.Min oscillator | MinE | MinD | conformational dynamics | self-organization

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“…MinE forms a ring that oscillates toward one pole and then to the other (337). It effectively sweeps the MinCD complex from one pole to the other by activating the ATPase of MinD, thereby causing MinD to hydrolyze ATP and thus release from the polar membrane (249,462). The net result from this negative regulator oscillating from pole to pole is a gradient of inhibi- tion that is highest at the poles and least at the midcell (335,336).…”

Section: What Are the Negative Regulators Of Ftsz Assembly?mentioning

confidence: 99%

Bacterial Growth and Cell Division: a Mycobacterial Perspective

Hett

Rubín

2008

Microbiol Mol Biol Rev

341

293

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SUMMARY The genus Mycobacterium is best known for its two major pathogenic species, M. tuberculosis and M. leprae, the causative agents of two of the world's oldest diseases, tuberculosis and leprosy, respectively. M. tuberculosis kills approximately two million people each year and is thought to latently infect one-third of the world's population. One of the most remarkable features of the nonsporulating M. tuberculosis is its ability to remain dormant within an individual for decades before reactivating into active tuberculosis. Thus, control of cell division is a critical part of the disease. The mycobacterial cell wall has unique characteristics and is impermeable to a number of compounds, a feature in part responsible for inherent resistance to numerous drugs. The complexity of the cell wall represents a challenge to the organism, requiring specialized mechanisms to allow cell division to occur. Besides these mycobacterial specializations, all bacteria face some common challenges when they divide. First, they must maintain their normal architecture during and after cell division. In the case of mycobacteria, that means synthesizing the many layers of complex cell wall and maintaining their rod shape. Second, they need to coordinate synthesis and breakdown of cell wall components to maintain integrity throughout division. Finally, they need to regulate cell division in response to environmental stimuli. Here we discuss these challenges and the mechanisms that mycobacteria employ to meet them. Because these organisms are difficult to study, in many cases we extrapolate from information known for gram-negative bacteria or more closely related GC-rich gram-positive organisms.

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MinC Mutants Deficient in MinD- and DicB-Mediated Cell Division Inhibition Due to Loss of Interaction with MinD, DicB, or a Septal Component

Cited by 61 publications

References 42 publications

The heat-shock response of Listeria monocytogenes comprises genes involved in heat shock, cell division, cell wall synthesis, and the SOS response

The heat-shock response of Listeria monocytogenes comprises genes involved in heat shock, cell division, cell wall synthesis, and the SOS response

MinE conformational dynamics regulate membrane binding, MinD interaction, and Min oscillation

Bacterial Growth and Cell Division: a Mycobacterial Perspective

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