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Sanjay Kumar

Sanjay Kumar has 2 articles published.

Mycobacteriophages and their potential as source against Mycobacterial active biomolecules

in Bioinformatics News/Genomics by

So, today is the great festival of Christmas……! Birthday of The Son of God.. And on this Auspicious day, We want to present before you all the power of Nature… How nature itself provides solution against the problem raised within it….. We all are aware of the epidemics of threat created by Mycobaterium tuberculosis and other related species. But, down here in this article we show how nature provides the solution against it.

As we know Bacteriophage (Bacterio= Bacteria’s, Phage= eater) infects several bacterium species. In contrast to it, a Mycobacteriophage is a member of a group of bacteriophages that infect mycobacterial species as their hosts e.g.,  Mycobacterium smegmatis and Mycobacterium tuberculosis, the causative agent of tuberculosis.

The rising incidence of tuberculosis, emergence of multi drug resistance in Mycobacterium tuberculosis and a slow progress in finding new drugs makes mycobacteriophage a potential candidate for its use as a diagnostic and therapeutic tool against TB.

All the characterized Mycobacteriophages are double-stranded DNA (dsDNA) tailed phages belonging to the order Caudovirales. Most are of the family Siphoviridae , characterized by  long flexible non contractile tails, whereas phages of the family Myoviridae, have contractile tails. There is a notable absence of mycobacteriophages from the family Podoviridae (containing short stubby tails), arising the question whether long tails are needed to traverse the relatively thick mycobacterial cell envelope. dsDNA tailed phages are either temperate, forming stable lysogens with a turbid plaque or lytic, forming clear plaques in which the host cells are killed. Mycobacteriophages can also be studied by the morphology of the plaques which vary in size and shape. Plaque morphology also depends on the burst size, which is the number of phage particles released on the lysis of the infected bacteria.

Genometrics of 70 sequenced Mycobacteriophages

Since the mycobacterial cell wall consists of a mycolic acid rich Mycobacterial outer membrane, attached to an arabinogalactan layer that is in turn linked to the peptidoglycan, it poses significant challenge to the phages. This challenge is met by a set of proteins, namely Lysin B proteins that cleave the linkage of mycolic acids to the arabinogalactan layer, holins that regulate lysis timing, and the endolysins (LysinAs) that hydrolyze peptidoglycan.

Phages affect hosts with a holin-endolysin system essential for programmed lysis. Endolysin is  found to be associated with a protein component of the phage tail involved in facilitating the penetration of the murein during injection of the genome into the host. Holins are small membrane proteins that form holes in the membrane through which the endolysin can pass. Holins control the length of the infective cycle for lytic phages so as to achieve lysis at an optimal time.

Endolysins can be a source of potential antibacterial because of its specificity (targeting only a few strains of bacteria) and thus replacing antibiotics (which have a more wide ranging effect), their low probababilty of developing resistance in Mycobacterium and novel mode of action.

Bioinformatics can assist this particular field of research by finding several other proteins existing on this planet or to prepare other such options having similar pharmacophore (physical and chemical attributes) properties. We can demolish the various disease threats by using natural options provided to us and can remain healthy on this planet. The only point to be remembered for this is,


(A major part of this article consist of some texts copied from

Hatfull, Graham F. “Mycobacteriophages: genes and genomes.” Annual review of microbiology 64 (2010): 331-356.

for any other information related references and queries, please let us know at [email protected]

Cancer: From the Eyes of Mathematical/Systems Biology

in Cancer/Systems Biology by

The month of November has just arrived with its generic glimpse of winter. We welcome this month with an evergreen and hot topic of cancer research. This time we intend to introduce you to an old research topic with a new vision…..

Cancer being an ailment with no remedy of full confidence has been pursued as a career by a lot of researchers. A cell biologist says it is an uncontrolled proliferation (increase in number by division and growth) of cells, molecular biologists call it a mutant variety of some biomolecules forcing a cell to commit such an uncontrolled cell division cycle. But, how does a Systems Biologist see such kind of a problem? Let us try to pursue it in a different way.

Proteins if are not assigned some name based on their function or structure, scientists mark them according to their molecular weight, e.g. p53, p200, p19 etc. Scientists have proven an abnormally high expression of p53 protein in Cancerous cells/tissues. p53 protein is actually the reason behind those other proteins which regulate the cell cycle and makes it to divide in to two as a normal scenario, p53 also helps in the manufacture of its inhibitor named Mdm2 protein. In any case of mutation in p53, that leads the failure of abnormality recognition by p53, doesn’t lead to increase in p53 and consequently Mdm2, p21 and other p53 regulated proteins. And thus, the division of abnormal cells continues indefinitely and causes Cancer.

Chemical reactions involved

From a Mathematical Biology perspective, systems biologists form some ordinary differential equations that look like a mathematical formula. These mathematical formulae are actually nothing else than the representative of chemical reactions and their combinations occurring inside a cell. As in our previous blogs (by Fozail Ahmad), we have mentioned about how to combine the chemical reactions in a shape of Ordinary Differential Equations (ODEs) and about how we follow Zero-Order chemical kinetics (reaction rate doesn’t depend on any participating chemical), First-Order chemical kinetics (reaction rate depends on only one participating chemical) and Second-Order chemical kinetics (reaction rate depends on two or more participating chemicals) to form the equations. In addition to that, I would like to mention that there are some reactions which occur with the help of some biomolecular machineries. These machines (enzymes) just help the reactions to occur, but do not take part in it themselves and thus affect the reaction in a different form of kinetics as described by the combined work of German Scientist of Biochemistry Leonor Michaelis and Canadian Scientist of Physics Maud Menten in 1913.Connected Chemical reactions

So, in a normal cell, when p53 senses the danger and signals the Cell by increasing p21 to combine with PCNA (Proliferating Cell Nuclear Antigen – An enzyme that helps in cell division) it stops the cell division. This type of cell cycle division has been shown in one of the diagrams mentioned below, while for the mutated case of p53 where it can not sense the cellular damage and thus divides normally is also shown in one of the images above.

Stages of Mathematical Modeling

We have also mentioned a combined picture, which shows a referral of how different stages of Mathematical Biology looks like. These figures are in special contrast to Cancer cells and normal cells.


Reference: Alam MJ, Kumar S, Singh V, Singh RKB (2015) Bifurcation in Cell Cycle Dynamics Regulated by p53. PLoS ONE 10(6): e0129620. doi:10.1371/journal.pone.0129620

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