cell biology and cellular processes vol 2 issue 2

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Cell Biology and

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Biotechnology, CSIR-Institute of Himalayan Bioresource Technology, Himachal Pradesh,

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Sangivalasa, Visakhapatnam (A.P.), India

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/University College of Medicine [UCM], Kolkata, India

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Research Institute Karnal (Haryana), India

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Nagarjuna University, Guntur (DT), India

Dr. Venu Perla West Virginia State University Research &

Development Corporation, Washington, USA

Dr. Avinash Tiwari School of Studies in Botany, Jiwaji University,

Gwalior, India

Dr. Sanjay Mahendrakumar Dave Department of Biotechnology,

Hemchandracharya North Gujarat University, Gujarat, India

Dr. Sukhjeet KaurDepartment of Biotechnology, SUS College of Engineering and Technology, Tangori-Mohali,

India

Dr. Anjali PriyadarshiniDepartment of Biotechnology,

PGIMER, Chandigarh, India

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CBIT, Hyderabad, India

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EDITORIAL BOARD MEMBERS

Dr. Aseel Mahmood AljamaliSurgery Department, College of Medicine,

Kufa University, Iraq

Dr. M. Anusuyadevi JayachandranMolecular Gerontology Laboratory,

Department of Biochemistry, Bharathidasan University, Tamil Nadu, India

Dr. Guru PrasadBasavatarakam Indo-American Cancer Hospital

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Dr. P. Udaya SriDepartment of Biotechnology, Acharya Nagarjuna University, Andhra Pradesh,

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Dr. Vishwas Tripathy Assistant Professor, Gautam Buddha

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Dear Readers,

We would like to present, with great pleasure, the Second Volume of a new scholarly

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Processes issues, from theoretical aspects to application-dependent studies and the

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cell, Eukaryotic and prokaryotic cell, Cell communication, Cellular senescence‎, Cell growth,

differentiation, migration, Signal transduction, Protein secretion and transport, Gene expression and

regulation, Cell-matrix interactions etc.

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It is our hope that this fine collection of articles will be a valuable resource for Cell Biology and Cellular

Processes readers and will stimulate further research into the vibrant area of Cell Biology and Cellular

Processes.

Puneet Mehrotra

Managing Director

1. Role of Fungus and Mycotoxins in the Genesis of the Breast Carcinoma A. Ravi Shankar, R. RajKumar, K. Rutu Raj, M. Guru Prasad 1

2. Overview of Cell Signaling Anuradha Chaudhary 9

3. New Switch Decides Between Genome Repairs, Death of Cells: A ReportShaina Chaudhary 16

4. Structure of an Anti-CRISPR ProteinAnuradha Chaudhary 17

5. Short Communication: How HIV Destroys Immune Cells?Manjit Singh 22

Contents

IJCBCP (2016) 1-8 © JournalsPub 2016. All Rights Reserved Page 1

International Journal of Cell Biology and Cellular Processes Vol. 2: Issue 2

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Role of Fungus and Mycotoxins in the Genesis of the Breast

Carcinoma

A. Ravi Shankar, R. RajKumar, K. Rutu Raj*, M. Guru Prasad Department of Microbiology, Kamineni Academy of Medical Sciences and Research Centre, Telangana, India

ABSTRACT

The commonest cancer in the world affecting the women after cervical carcinoma is the breast cancer. The etiology for the genesis and progression of breast cancer includes mutations and infectious agents including oncogenic viruses and fungi. The role of oncogenic viruses in the formation of breast carcinoma is known. We reviewed the possible role of the fungi or mycotoxin and carcinogenic mechanism in breast cancer formation. Keywords: BRCA1, BRCA2, mycotoxins, TGF-2

INTRODUCTION

Fungi are the large group of eukaryotic organisms including yeasts, molds as well as edible mushrooms. These organisms were different from others in having the presence of chitin in their cell wall. Fungi were very abundant in nature and spread worldwide and act as symbionts, nonpathogenic and pathogenic organisms. They play an important role in the organic matter decomposition in nature, fermentation of the various food products, production of antibiotics etc. On the other hand fungi acts as major pathogens or the agents causing disease in humans, and it is collectively termed as the mycoses, similarly the exposure of skin, or diet to the toxic fungal metabolites leads to a condition termed as mycotoxicoses.[1].These fungi or mycotoxins termed as hidden killers, they cause a number of infections in numerous organs of the body. It includes dermatophytes causing athletes foot, or infection to nails.[1] The invasive fungal infections are mainly caused by Cryptococcus, Candida, Aspergillus sp. The fungal pathogens such as Cryptococcus sp. were classified as the primary pathogen which causes disease

leading to the development of subclinical disease.[2]

These opportunistic pathogens incite disease in patients with impaired immune system. The virulence factors which contribute for the development of the mycoses includes the adherence to the tissues by the fungus involving the a cell wall molecule adhesion, which resist the physical clearing the fungus in the humans, for example Histoplasma capsulatum and Candida albicans adhere to various host surfaces, avoid being washed out and initiates the onset of hematogenous infections.[2] The other mechanism includes the presence of penetration and dissemination factors. The Aspergillus fumigatus has an ability to penetrate the blood vessels and disseminate through blood.[3] The necrotic enzymes produced by the fungus such as extracellular proteinase produced by the C. albicans, Aspergillus sp. allow the fungus to overcome structural barriers. The other

IJCBCP (2016) 9–15 © JournalsPub 2016. All Rights Reserved Page 9


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Overview of Cell Signaling

Anuradha Chaudhary Department of Biotechnology, Lovely Professional University, Punjab, India

Cells regularly convey utilizing chemical signals. These chemical signs, which are proteins or different molecules produced by a sending cell, are regularly discharged

from the cell and discharged into the extracellular space. There, they can float – like messages in a bottle – over to neighboring cells.

Sending cell: this cell secretes a ligand Target cell: this cell has a receptor that

can tie the ligand. The ligand ties to the receptor and triggers a signaling cascade inside the cell, prompting to a response.

Non target cell: this cell does not have a receptor for the ligand (however it might have different sorts of receptors). The cell does not see the ligand and in this manner does not react to it.

Not all cells can "hear" a specific chemical message. In order to detect a signal (that is, to be a target cell), a neighbor cell must have the correct receptor for that signal. At the point when a signaling molecule ties to its receptor, it adjusts the shape or movement of the receptor, triggering off a change within the cell. Signaling particles are regularly called ligands, a general term for molecules that predicament particularly to different molecules, (for example, receptors). The message conveyed by a ligand is frequently handed-off through a chain of chemicals messengers inside the cell [1].

At last, it prompts to an adjustment in the cell, for example, modification in the movement of a gene or even the acceptance of an entire procedure, for example, cell division. In this manner, the first intercellular (between-cells) signal is changed into an intracellular (inside cell) signal that triggers a reaction.

Types of Signaling

Cell-cell signaling includes the transmission of a signal from a sending cell to a receiving cell. Notwithstanding, not all sending and receiving cells are nearby neighbors, nor do all cell pairs exchange signals in the same way.



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New Switch Decides Between Genome Repairs, Death of Cells: A

Report

Shaina Chaudhary Department of Microbiology, Lovely Professional University, Punjab, India

The genetic information of each cell is encoded in the sequence of the DNA double helix. Double strand breaks up the DNA, which can be instigated by radiation, are a dangerous threat to the cells, and if not appropriately repaired can prompt to cancer. Damaged cells need to choose whether the breaks can be settled or whether they ought to be evacuated by a cellular suicide program called "apoptosis" before starting cancer. The genetic information of each cell is encoded in the sequence of the DNA double helix. Double strand breaks up the DNA, which can be initiated by radiation, are a dangerous danger to the cells, and if not appropriately repaired can prompt to cancer. Damaged cells need to choose whether the breaks can be settled or whether they ought to be evacuated by a cellular suicide program called "apoptosis" before starting cancer. Björn Schumacher, one of the senior authors, clarifies: "Inside seconds after an unsafe episode, diverse instruments begin. Schizophrenically, the cells begin repairing and in preparing for apoptosis. We recognized an uncharacterized system that incorporates signals from the continuous repair handle and the cell death machinery. A protein called UFD-2 frames expansive edifices at the breaks and verifies whether to proceed with the repair or whether it's time to die." Simultaneously, UFD-2 is a point of intersection that both gets and gives signals. The tests were performed with the nematode Caenorhabditis elegans. "For our research we utilized diverse strains of C. elegans, including wild sort and genetically modified ones. They were presented to ionizing

radiation to instigate double strand breaks and afterward analyzed," says Leena Ackermann, lead author of the review. Schumacher includes: "The outcomes are imperative to additionally see how and why a cell chooses to repair or to die. Is the repair as yet continuous and effective or is apoptosis essential? Cells lacking UFD-2 neglect to experience apoptosis. In people such a circumstance could prompt to a higher danger of a damaged cell turning into a cancer cell." All the proteins that have an influence in this mechanism can be found in humans also, and the discoveries could be exceptionally applicable to better seeing how DNA damage prompts to cancer. DNA damage is likewise an imperative driver of the aging process. Despite the fact that apoptosis protects from cancer, excessive cell death can prompt to tissue degeneration and aging. The senior author Thorsten Hoppe initially distinguished UFD-2 as a key regulator of protein degradation. Here, UFD-2 frames administrative focuses that facilitate DNA repair and cell death. Hoppe seeks after coming about advances in tumor therapy: "The information we picked up from this review gives new points of view to fighting cancer pharmaceutically. It may be conceivable to control the very much balanced process of apoptosis and protein degradation to make clearance of tumor cells more proficient."



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Structure of an Anti-CRISPR Protein

Anuradha Chaudhary* Department of Biotechnology, Lovely Professional University, Punjab, India

ABSTRACT

Bacterial CRISPR–Cas adaptive immune systems utilize small guide RNAs to protect against phage infection and invasion by outside genetic components. We heretofore showed that a get-together of Pseudomonas aeruginosa phages encode against CRISPR proteins that inactivate the type I-F and I-E CRISPR–Cas frameworks using particular mechanisms. Here, we present the three-dimensional structure of a hostile to CRISPR protein and guide a valuable surface that is essential for its powerful inhibitory action. The connection of the counter CRISPR protein with the CRISPR–Cas complex through this utilitarian surface is proposed to keep the binding of target DNA.

Keywords: bacteria, DNA, RNA

INTRODUCTION

Phage predation is a major selective pressure on bacterial populaces, and bacteria have advanced an evolved an adaptive immune system, known as CRISPR–Cas, to shield against them. CRISPR loci are included palindromic repeats sequences blended with novel short spacer districts that are regularly identical to phage and plasmid deoxyribonucleic acid (DNA) After transcription, CRISPR ribonucleic corrosive (RNA) is prepared and complexed with Cas proteins to frame a genome reconnaissance system guided by the sequence of the spacer RNA. Sequences particular authoritative by this complex to an invading phage genome targets it for degradation. AcrF1, is a strong inhibitor of the type I-F CRISPR–Cas system of P. aeruginosa. AcrF1 hinders the DNA- binding activity of the reconnaissance complex of this system (called the Csy complex) by communicating with the Csy3 subunit6 [1, 2]. Using site-directed mutagenesis, recognize a practical surface through which it intervene its hostile to CRISPR

movement. The inactivation of the type I-F CRISPR–Cas system by AcrF1 was observed to be reliant on tight official to the Csy complex. LOCUS STRUCTURE

Repeats and Spacers

CRISPR repeats extend in size from 24 to 48 base pairs. They more often than some dyad symmetry, inferring the arrangement of an auxiliary structure, for example, a hairpin, yet are not really palindromic. Repeats are isolated by spacers of comparable length. Some CRISPR spacer sequences precisely coordinate arrangements from plasmids and phages, although some spacers coordinate the prokaryote's genome (self-targeting spacers) [3]. New spacers can be included quickly as a major aspect of the immune response to phage infection. Cas Genes and CRISPR Subtypes

Small clusters of cas genes are frequently situated alongside CRISPR repeat-spacer arrays. Similar genomics identified multiple cas genes; an underlying analysis



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Short Communication: How HIV Destroys Immune Cells?

Manjit Singh Department of Biotechnology, DAV College, Punjab, India

HIV leads to AIDS principally because the virus destroys essential immune cells called CD4 T cells, but precisely how these cells are killed has not been clear. Two papers written by same G. Doitsh et al. and K. M. Monroe et al. reveal the molecular components that cause the death of most CD4 T cells in lymphoid tissues, the main reservoir for such cells, during infection. Two research groups led by Warner Greene at the Gladstone Institutes in San Francisco have exhibited that by far most of CD4 T cells in lymphoid tissues despite their ability to resist full infection by HIV, respond to the presence of viral DNA by relinquishing themselves by means of pyroptosis – a highly inflammatory form cell death that lures more CD4 T cells to the area, in this manner making an endless loop that eventually wreaks havoc on the immune system. "It's truly elegant science," said Anthony Fauci, director of the National Institute for Allergy and Infectious Diseases at the National Institutes of Health (NIH) in Bethesda, Maryland, who was not included in the research. "It goes far to clarifying what has been a puzzle for all intents and purposes 30 years." Richard Koup, who drives the immunology lab at the Vaccine Research Center at the NIH, concurred: “For a considerable length of time we have recently said ‘HIV infects the cells and kills them,’ however it's obviously more complicated than that. These papers begin to depict the numerous diverse

components that HIV may need to slaughter CD4 T cells” [1]. “This cell-death pathway interfaces the two signatures of HIV Research Center that is, CD4 T cell-depletion and chronic inflammation surprisingly,” included Greene, who coordinates the Gladstone Institute of Virology and Immunology. Besides, existing anti-inflammatory can hinder the pathway, raising the possibility of new therapies that objective the host reaction as opposed to the virus. The death of CD4 T cells amid HIV infection has by and large been credited to plain old apoptosis, or customized cell death. Issue is, most reviews have concentrated on active cells in the blood, which are “productively infected “by HIV, implying that the virus has incorporated with host-cell genome and can make duplicates of itself. In a recent report, Greene and his associates demonstrated that 95 percent of CD4 T cells in lymphoid tissue, by differentiation, are bystander cells that are " abortively infected "– the virus penetrates however can't coordinate or repeat. To better comprehend HIV pathogenesis, Greene tried to make sense of how this specific populace of immune cells dies during HIV infection. G. Doitsh et al. looked at human spleen and tonsil tissue refined in the lab and spiked with HIV. The scientists found that when the virus productively infects the couple of permissive CD4 T cells present, death happens through apoptosis intervened by a protein called caspase-3. Be that as it may, when HIV abortively

International Journal of

Cell Biology and

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Electrical Engineering« International Journal of Analog Integrated Circuits« International Journal of Automatic Control System« International Journal of Electrical Machines & Drives« International Journal of Electrical Communication

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