Colonizing Mars! Lessons on avoiding inbreeding issues from flatworms by Longhua Guo!

Imagine the year 2500. We have chosen twenty of our best and brightest to send to Mars. They have the mission to start a human colony there. Of-course that would mean breeding and generating more humans. But with only 20 people, the population might be genetically too small. Creating babies from genetically similar individuals, like cousins, can lead to birth defects. Within a few populations, intermixing might doom the entire project, just like inbreeding doomed the once powerful Habsburg Dynasty. How can we avoid this?

The question is not only critical to our hypothetical journey to Mars, but also to survival of critically endangered species. Very few individuals of hawksbill turtle, tigers and many other remain. How can we avoid in-breeding defects in such animals in near future. The answer to that might lie in the champions of regeneration, freshwater planarians. Planarians are known for their amazing capacity to regenerate a full animal from any part of their body. But also, as Longhua and colleagues found out, can avoid their genome from becoming similar after multiple rounds of in-breeding. How can these animals achieve such feat, please listen to Longhua to know more:


For more information, please refer to:
Widespread maintenance of genome heterozygosity in Schmidtea mediterranea.
Guo L., et al., Nature Ecology & Evolution, 2016.

Further information can be found here:
The joy of figuring things out: a story of worms, haplotypes & genetic ancestry.

Eat me not! Interview with Anu Chaudhary on cell surface marker regulating autophagy in humans!

Cells are constantly talking with each other, mostly with the help of cell surface receptors and ligands. This includes information on the amount of 'self-digestion' to perform. Higher self-digestion, or autophagy, leads to faster protein turnover and has been implicated in many age-related diseases, esp. those with an autoimmune component. Could we understand the mechanism controlling levels of autophagy and modulate it to affect disease outcomes?

Anu Chaudhary and her colleagues display an elegant way to screen human genetic variation underlying any observable phenomena. By focusing on response to rapamycin, a drug that induces autophagy, they were able to isolate variations that enhance cellular self-digestion. They use this to characterize cell surface receptors that can vary autophagy levels, and use this knowledge to develop means that could deter auto-antibody production. To learn more about the exciting and relevant finding, please listen to Anu.


For further information, please refer:
Human Diversity in a Cell Surface Receptor that Inhibits Autophagy.
Chaudhary et al., Current Biology, 2016.

Finding causative needle in genomic haystack -- Interview with Samuel Tsang about drivers of Pancreatic Caner!!

Pancreatic cancer is the deadliest kind, with only 5% people surviving after 5 years from diagnosis. Many celebrities including Steve Jobs and Patrick Swayze succumbing to it. Pancreatic cancer, like any other, is a heterogeneous disease with many cell and gene of origins leading to its development and spread. But how can doctor find out the cause behind his patient's pancreatic cancer. Could there be a fast and efficient way to screen for the causative needle in the genetic haystack.

Samuel Tsang and his colleagues wanted to develop a method that could do exactly that. They develop a mouse model based protocol capable of testing the cancer causing capacities of genetic variations within a human patients. To know more about the technique, please listen it.



Please refer to the following article for more information:
Functional annotation of rare gene aberration drivers of pancreatic cancer.
Tsang et al., Nature Communications, Jan. 2016.