Basic Details

Roll No
Name ISHITA MALIK
Native INDIAN
Subject in M.Sc. BOTANY
Marks (%)/CGPA in M.Sc. 8.23
University JAMIA HAMDARD
Year of Passing PG 2020
MSc dissertation/thesis topic (if any) Prediction of Plum Pox derived
siRNAs and their possible impact
on the ABC and monosaccharide
transporter
NET/GATE/JRF GATE Score - 387
CUCET Score (if applicable) NA
Experience post PG (if any) NA
If selected in more than one department 1. Microbiology
(Microbiology, biotechnology, 2. Biotechnology
biochemistry, nutrition biology), please 3. Biochemistry
provide the order of choice for admission 4.
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 Title of Proposed Doctoral Work

• To treat infectious diseases caused by Methicillin drug-

resistant Staphylococcus aureus using the Quorum quenching
mechanism.
 Background of the Problem
Quorum-sensing (QS) is the ability of microorganisms to sense the bacterial cell density and respond with gene expression changes. It plays a
central role in the pathogenesis of Staphylococcus aureus via the accessory gene regulator (Agr). QS controls virulence factors such as hemolysins,
leukocidins, cell surface adhesins, exoenzymes, and biofilm formation via the Agr, which relies on the auto-inducing peptide (AIP).
Two primary transcripts, RNAII and RNAIII, are generated by the agr and originate from the P2 and P3 promoters. The P2 operon encodes four
proteins that generate the Agr-sensing mechanism. AgrB is a transmembrane protein that appears to be involved in the processing of the agrD
product into an octapeptide, secretion and modification of the autoinducing peptide (AIP).
AgrA and AgrC form a two-component regulatory system in which AgrC (histidine kinase) binds the extracellular AIP and modulates the activity of
AgrA, leading to significantly increased P2 and P3 transcription. Increased transcription of the P3 results in dramatically increased intracellular
RNAIII, which encodes the toxin δ-hemolysin and increases the transcription of several secreted virulence factors.
To interfere with QS, bacteria use quorum sensing inhibitors (QSIs) to block AIPs and quorum quenching (QQ) enzymes to degrade signaling
molecules. QQ can be developed as a technique for disrupting the ability of a pathogen to sense its cell density and disable the capability of
triggering the virulent expression. QQ enzymes and other QS blocking approaches do not kill pathogens but instead block virulence factor
production and such methods impart less selective pressures that lead to the development of resistant mutant.
Targeting AIPs carries the advantage of influencing QS extracellularly and potentially avoiding complications of cellular uptake and degradation
that intracellular therapies may encounter. Due to the more extensive use of antibiotics, bacteria have become resistant to
antibiotics & thus, to control them, various unconventional strategies have been employed. One of these strategies is to impede the mechanism of
Quorum Sensing.
Quorum sensing is based upon Gene Regulation in which bacteria synchronize the expression of specific genes in response to the presence or
absence of small signal molecules.
 Tentative Objectives

• To find out the possible compounds or chemicals which can be used as

inhibitors to signaling molecules of Staphylococcus aureus and prevent
its Quorum sensing mechanism
• The possible ways and future prospects to detect the
compounds/chemicals/enzymes involved in inhibition of Quorum
sensing
• Predict the phenomenon of Quorum Sensing by In-Silico studies.
 Expected Outcomes

• The control bacteria is able to produce virulence factors while their

level in the transformants is reduced significantly.
• This is because the phosphorylation of TRAP is essential to create
autoinducing loop which leads to the activation of RNAIII synthesis.
• Because this method is different from conventional antibiotic
therapy, which kills bacteria by interfering with DNA, RNA or protein
synthesis, leading to the emergence of antibiotic-resistant superbugs,
QQ is a promising approach that may lead to the development of very
effective next generation antibacterial drugs.