Give me food, give me sex; give me that which I desire -- Interview with Yi Li about reward sensing!!

Chocolate, chips, cigarettes, alcohol, sex; well, we all choose our sins. What is making us crave for such desires, and what happens when we finally achieve them. Yi Li in his exciting study published in Nature Communications shows that serotonergic neurons in the dorsal raphea nucleus in brain might be involved in reward and pleasure behavior. He did this by observing and recording neuronal activity in live, uninhibited mice while they seek food, sucrose, social interaction and even sex. We call him to hear more about this exciting study.   

You can read the original article here: 

Serotonin neurons in the dorsal raphe nucleus encode reward signals

Li et al., Nature Communications 7, 10503, January, 2016.

Selfish beta-cells and Motor Neurons going both ways - Chat with Theresa Hartmann

You might have all heard about the 'Selfish gene', the groundbreaking unconventional hypothesis published 40 years ago by Richard Dawkins. But, did you know that cells can also become selfish under stress.
Theresa Hartmann summarizes an article, Evidence of β-cell Dedifferentiation in Human Type 2 Diabetes, that suggests that β-cells - the cells that produce insulin for regulation of blood glucose and whose defects lead to diabetes, could act selfishly under stress!!
β-cell stress can occur due to large workload thrust upon them due to obesity or insulin resistance -  the case where body organs cannot properly sense insulin and thus demand more of it. This makes them sick over time and ultimately kills them. To escape this adverse end, a few of these cells lose their identity; they 'forget' who they are supposed to be; and become something else. They no longer sense metabolic stress and can continue to survive. Of course, this occurs at the cost of the person's health which deteriorates faster from even lower β-cell mass.

Next, I help summarize a fascinating discovery that might upturn hundred year old belief. It has been always thought that motor neurons -  the cells that connect the brain to the muscle, only pass signals in one direction. They act as passive relays of the message from the information and processing centers to the acting musculature. But new research, Motor neurons control locomotor circuit function retrogradely via gap junctions, suggests that this might be so simple. The article suggests that the motor neurons are connected to the upstream processors with gap junctions - proteins that connect the cytoplasm of two cells allowing free movement of molecules and ions between two cells. Such connection allows motor neurons to communicate, and control, the activity of higher processing units, thus making the connection from brain to muscles two directional.

Please have a listen!

In case of heart problems, call 1-800-BMP-Caveolin - Interview with Chi-Chung Wu and Jingli Cao

Today our attention turns to heart disease, one of the leading cause of death in the world. Upon heart attack, cardiomyocytes, or the heart muscle cells die off, and this loss is irreversible. As time passes, the lack of heart muscle stresses the organ finally leading to failure. On the other hand, zebrafish posses extraordinary capacity to recover from strong cardiac trauma. We talk to two scientists, Chi-Chung Wu from Ulm University and Jingli Cao from Duke University, who have recently shown how the zebrafish is capable of doing so.

Both the studies share certain commonalities:

Firstly, in order to understand the system they both use novel cutting edge methodology to look at RNA – the middle man between DNA, the information component of the cell, and protein, the functional component of the cell. While Chi-Chung probes the RNA landscape to find genes involved within the heart cells at the injury site, Jingli looks at RNA content within single cells of the epicardium, a sheet covering the heart wall.

Secondly, both authors find factors that are dispensible for development, but become initiated by tissue damage and are necessary for successful recovery. One might think the extraordinary capacity of the zebrafish to regenerate its organs might lie in such genetic differences post-injury. To learn more about the process, please listen to the podcast.

To know more about the work, please read the articles:

Spatially Resolved Genome-wide Transcriptional Profiling Identifies BMP Signaling as Essential Regulator of Zebrafish Cardiomyocyte Regeneration.
Wu, Kruse et al., Developmental Cell, 2016, 36-1: p36–49.

Single epicardial cell transcriptome sequencing identifies Caveolin 1 as an essential factor in zebrafish heart regeneration.
Cao et al., Development, 2016 143: 232-243.

Cheaters Make Co-operation Robust!

Which of these is true??

1. You need rational beings with minds to have teamwork.
2. Bacteria and yeast, organisms without brain, cannot collaborate for the good of each other.
3. Cheating individuals destroy co-operation in the society, and crash its existence.

If you thought that all were false, you might be in for a surprise!

We do have limited resources in this world. And for our survival, correct utilization of those resources based is of utmost importance. Many people can co-operate peacefully with each other to manage resource use. 

But what happens when a few people start to cheat, and greedily take more than their fair share without contributing to the general good. One would think this would cause havoc and destroy the delicate balance of co-operation among individuals, finally leading to population crash. 

Unexpectedly, Adam Waite in his work performed at University of Washington found otherwise. He simulated population dynamics between co-operative and cheating individuals sharing limited resources, and excitingly found that the population became more robust to crashes. 

To understand this exciting and interesting finding, lets call him up!

To know more about the work, please read the article:
Defectors Can Create Conditions That Rescue Cooperation
Waite et al., PLOS Computational Biology 11(12): e1004645, December, 2015.

and the blog:
Cheaters allow cooperators to prosper

How we sense hunger? Interview with Zhiying Li.

What tells our body that it needs food?? The answer might lie within the working of a hormone called leptin. The hormone, mostly secreted by fat tissue, works on a small area of the brain, the hypothalamus, to control hunger and satiety. Its decrease leads to over-eating and obesity. Now, Zhiying, a post-doc in Jeffery Friedman's Lab at Rockefeller University, finds that the molecule might have a brother-in-arms for control of such feelings. In her article published in Cell Metabolism, she finds that another peptide hormone, amylin, works in concert with leptin and enhances its effect. Combinational therapy with both amylin and leptin seem to have better effect on controlling obesity. We ring her up and try to find more about this new synergy!


Read the article for yourself:
Hypothalamic Amylin Acts in Concert with Leptin to Regulate Food Intake
Li et al., Cell Metabolism, Dec. 01, 2015.

Call with Arjun Raj

Today we call Dr Arjun Raj from UPenn to discuss cellular heterogeneity: how seemingly similar cells might be very different from each other if looked at closely. We also talk about scientific method and training; guidelines for scientist at any stage.

Please listen.

To learn more about Arjun Raj's work, visit his lab website.


Citations:
Stochastic mRNA synthesis in mammalian cells
Raj et al., PLoS Biol., October 2006.

Half dozen of one, six billion of the other: What can small- and large-scale molecular systems biology learn from one another?
Genome Research, October 2015.

Top 10 signs that a paper/field is bogus

Call with David Matus

We interview Dr David Q. Matus to discuss how studying a single cell within a simple worm informs us about cancer metastasis and might help with developing better treatments against the disease.

David recently started his own lab in the department of Biochemistry and Cell Biology at Stony Brook University in New York. As a post-doc in the lab of Dave Sherwood at Duke University, Dave studied the anchor cell in the worm C. elegans. The anchor cell invades by breaching the basement membrane; a process very similar to what is used by cancer cell for metastasis. David found interesting link between cell cycle and the invasion behavior. His study suggests a requirement of cell cycle arrest for membrane invasion. This interesting link could be one reason why chemotherapy, which is directed towards killing dividing cells, fails to destroy all cancer cells. Metastasizing cells due to their inhibition of cell cycle, escape chemotherapy. Understanding the properties underlying invasion could lead to developing better compounds targeting the spread of cancer cells.

Please listen.

To learn more about David, visit his lab webpage.



Citations:
Invasive Cell Fate Requires G1 Cell-Cycle Arrest and Histone Deacetylase-Mediated Changes in Gene Expression
Matus et al., Developmental Cell, October 26, 2015.

Cell division and targeted cell cycle arrest opens and stabilizes basement membrane gaps
Matus et al., Nature Communications, June 13, 2014.