Bacterial Growth and Cell Division: a Mycobacterial Perspective
Erik C. Hett and Eric J. Rubin



SUMMARY
INTRODUCTION
CELL WALL COMPONENTS
What Is the Structure of the Mycobacterial Cell Wall?
PG.
AG.
MAs.
Are Mycobacteria Gram Positive or Gram Negative?
Why Are Mycobacteria So Innately Resistant to Antibiotics?
If Mycobacteria Are So Impermeable, How Do They Access Nutrients?
How Do Mycobacteria Synthesize Cell Wall Components?
PG.
AG.
MAs.
How Is PG Synthesis Controlled?
What Regulates the Activity of Enzymes Responsible for PG Synthesis?
Do Mycobacteria Recycle Cell Wall Material?
How Do Antibiotics Target the Cell Wall?
MAINTENANCE OF SHAPE
Why Are Mycobacteria Rods?
What Is the Role of PG in Determining Cell Shape?
Where Does Nascent PG Localize?
Is Inert PG Involved in Branching?
What Is the Role of the Cytoskeleton in Shape?
Tubulin.
Intermediate filaments.
Actin.
Why Do Mycobacteria Grow at the Tips?
What About Inert PG at the Tips?
How Can Mycobacteria Maintain Shape without MreB?
What Is Different about Mycobacterial Growth?
BACTERIAL CELL DIVISION
What Is the Order of Events in Cell Division?
How Does the Chromosome Replicate?
What Segregates the Chromosome?
What Are the Divisome Components, and How Do They Assemble?
What Is Missing in Actinomycetes?
What Are the Negative Regulators of FtsZ Assembly?
Min system.
Nucleoid occlusion.
How Does FtsZ Constrict?
How Does FtsZ Polymerize, and Why Is Mycobacterial FtsZ So Slow?
Is Growth Rate Related to Mycobacterial Pathogenesis?
What Hydrolyzes the Septal PG?
What Is the V-Snapping Process of Dividing Mycobacteria?
What Is Different about Mycobacterial Cell Division?
REGULATION OF BACTERIAL GROWTH AND DIVISION
What Are STPKs, and How Do They Work?
PknA and PknB.
Other STPKs.
How Are WhiB Proteins Involved in Growth Regulation?
CELL DIVISION UNDER SPECIALIZED CONDITIONS
How Is Entry into and Escape from the Dormant States Regulated?
TCSs.
DosRS/T dormancy phosphorelay system.
Other TCSs.
Alternative sigma factors.
What Else Is Regulated during Infection?
TA system.
What Is the State of Dormancy Models?
Stringent response.
How Do Mycobacteria Reactivate from Dormancy?
The Rpf story.
How Is Rpf Regulated?
How Could Rpf Activate Bacteria?
Does Resuscitation Involve Normal Homeostatic Processes?
CONCLUSIONS
ACKNOWLEDGMENTS
REFERENCES


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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