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Bacterial Growth

Increase in the number of cells in a population


What is the need of studying bacterial growth?
Cell division
DNA replication and cell elongation
Formation of cell division plane
Synthesis of petidoglycan
Cell division
Generation time: time required for one cell to divide and form two
cells
Binary fission
During growth cycle all cellular constituents increases proportionally
and each daughter cell receives chromosomes and sufficient copies of
ribosomes and other monomers.

What triggers cell division in bacteria?
How is it controlled?
In Rod shaped bacteria how constriction happens exactly at the
center ?


Control of Cell Division :
Fts Proteins and divisome
Min proteins (minicell locus ) Min C, Min D and Min E)
Nucleoid occlusion mechanism
Fts Proteins
Fts (filamentous temperature-sensitive)
Proteins
Essential for cell division in all prokaryotes
Interact to form the divisome (cell division
apparatus)
FtsZ: forms ring around center of cell
ZipA: anchor that connects FtsZ ring to cytoplasmic
membrane
FtsA: helps connect FtsZ ring to membrane and also
recruits other divisome proteins
Related to actin
FtsI peptidoglycan biosynthesis proteins
FtsK separates chromosome
DNA replicates before the FtsZ ring forms

Location of FtsZ ring is facilitated by Min proteins
(minicell locus )
MinC, MinD : Inhibits FtsZ anchoring
MinE : Inhibitor of MinC and MinD present at the center
FtsK protein mediates separation of chromosomes to
daughter cells
1. DNA replication and segregation
2. Min system controls the site of division
3. FtsZ ring assembly in the center along with
the formation of divisome
4. Z-ring maturation
5. Septal invagination with the constriction of
the envelope layers
6. Septum closure and splitting of the
daughter cells
FtsZ ring assembly
1. First group of proteins assembles and
anchor the FtsZ to form Z ring
2. Z ring forms as an arc at several points at
the median
3. Arc formed by the self polimerization of
FtsZ proteins with the help of GTP
utilization
4. FtsA and ZipA proteins anchor the micro
arc on the cell membrane
Z-ring maturation after orderly
recruitment of the divisome
components
1. By the ordered recruitment of late
divisome components
2. ZapA and ZapC enhance the
polymerization of the arc by
aggregating the FtsZ and inhibiting
GTPase activity.
3. FtsK drag Chromosome from the plane

Septal invagination with the constriction of
the envelope layers
Constriction is energy dependent
Z-ring can exert a constrictive force onto the
membrane
Simultaneously autolysin hydrolyses
peptidoglycan layer and create small opening on
the cell wall
New wall materials are added across the opening
with the help of bactoprenol and PBP

Control of Z ring assemly
By Two complementary systems ; Min system and Nucleoid occlusion

Min system prevents aberrant division at the poles
Fts inhibitor MinC and MinD organized to form MinCD complex
MinCD prevents the lateral assembly of FtsZ
Competes with FtsA and ZipA
Min E system prevents MinCD complex
Regulation of Z ring ASSEMBLY
Nucleoid occlusion
DNA associated proteins inhibits Z-ring formation
This provides a protective mechanism to the DNA, and contributes to the
precise temporal and spatial positioning of the division septum.
Growth rate dependent Z ring inhibitor
UgtP (UDP-glucose diacylglycerol glucosyltransferase) was identified
in B. subtilis and may constitute the link between
metabolism and cell division
Under nutrient rich conditions, in response to high levels of
its substrate, UgtP is present in the cytoplasm inhibits FtsZ
assembly, by disruption of the lateral protofilaments
interactions
during growth on a poor carbon source, the levels of UgtP
are reduced
When DNA is damaged, an SOS response is activated
to repair the DNA and cease cell division by inhibiting
FtsZ polymerization