A Bacterial Gene to Help Smokers Quit

-
Tobacco use represents a major worldwide health problem. Around one fifth of the world's population regularly smokes tobacco and nearly half of these people will die from tobacco-related illnesses (1). And yet, nicotine addiction is extremely difficult to overcome.

A study just published by Xue et al., from The Scripps Research Institute, describes a new biochemical tool that could eliminate the addictive power of nicotine, and make quitting much easier (2).

This team of biologists and chemists made use of bacteria known as Pseudomonas putida, isolated from tobacco fields (3). These bacteria consume nicotine as a food source, and an enzyme known as NicA2 is a primary component of their nicotine metabolism. Using a gene from P. putida, Xue et al. were able to purify recombinant NicA2 enzyme capable of degrading nicotine. They anticipate that the NicA2 enzyme may soon be used as a treatment for nicotine addiction. The hope is that NicA2, if administered to smokers, could destroy nicotine in the blood before it ever has a chance to reach the brain and deliver its "rewards." The next logical steps will be to test NicA2 in vivo. This could be done either by using the recombinant enzyme, or by expressing the NicA2 gene in animals subject to nicotine treatment.

Reference

1. World Health Organization, Global Health Observatory (GHO): http://www.who.int/gho/tobacco/
2. Xue, S., Schlosburg, J. E., & Janda, K. D. (2015). A new strategy for smoking cessation: Characterization of a bacterial enzyme for the degradation of nicotine. Journal of the American Chemical Society.
3. Wang, S. N., Liu, Z., Tang, H. Z., Meng, J., & Xu, P. (2007). Characterization of environmentally friendly nicotine degradation by Pseudomonas putida biotype A strain S16. Microbiology, 153(5), 1556-1565.
Original Source: Cyagen Biosciences

Comments

Post a Comment

Popular posts from this blog

Knockout by CRISPR vs Knockdown by shRNA

-
In solving the mystery of gene function, there is no more important clue than the phenotype of inactivating the gene of interest. With a plethora of methods available, researchers must first determine what approach is best for their specific scientific questions and experimental systems. For over a decade, RNA-interference-based methods of gene knockdown (i.e. RNAi & shRNA) have provided a wealth of insight into gene function, but in recent years the advent of CRISPR- and TALEN-based methods now allow genome editing to be used to quickly and efficiently test the effect of gene knockouts. Here, we review the advantages and disadvantages of these approaches, and describe some experimental situations in which one approach is better than another, focusing primarily on CRISPR/Cas9 and shRNA. For a discussion of the relative advantages of CRISPR/Cas9 versus TALEN , see our prior Newsletter on this topic. CRISPR Knockout In this method, a guide RNA (gRNA) homologous to an 18-22nt ta...
Read more

Extending Lifespan of Mice, Then Human

-
Image
Invariably, everyone gets old. However, as a true testament to human stubbornness, research toward a “cure” for aging has never stopped. Over the past few decades, various approaches have allowed scientists to generate animal models with extended lifespans. In recent years, this trend has moved from lower organisms to mammalian model systems. There are now several rodent models with enhanced longevity. Many of these models are directly relevant to human aging. A new study has identified a deletion in exon 3 of human growth hormone receptor (GHR) to be prevalent in naturally long-lived men (1). The presence of two copies of this mutation may allow men to live about ten years longer than they otherwise would. This agrees with many findings from rodent models. Transgenic mice that overexpress GH age rapidly, while knockout mice lacking GHR are long-lived (2,3). In humans and mice, IGF1 signaling is also closely linked to longevity via a signaling pathway overlapping that of GH (4,5). ...
Read more

Healing a broken heart

-
Image
Introduction: Reduced heart function due to aging and disease is a major health problem. Heart attacks can have devastating impacts, often leading to the death of the patient or chronic morbidity for those that survive. A major reason for the sensitivity of the circulatory system to heart malfunction is that heart muscle cells (cardiomyocytes) of adult mammals generally do not divide. This means that when a cardiomyocyte dies, due to localized loss of blood supply, for example, that dead cell will never be replaced. Normally, heart tissue has a robust, healthy blood supply, but when a heart attack strikes, portions of heart tissue are deprived of blood flow, resulting in rapid cell death in those sections of the heart. Recovering the ability to heal Interestingly, newborn hearts can heal. In 2011, scientists discovered that newborn mice are able to regenerate cardiomyocytes to repair heart damage, but this ability is lost soon after birth (1). More recently, researchers disc...
Read more