For me, biology has always been an endless puzzle. Early in my career I was inspired by Jacques Monod’s famous maxim: “Tout ce qui est vrai pour le colibacille est vrai pour l’éléphant.” In English it is often rendered as “What is true for E. coli is true for the elephant.”1 During six years of graduate study, I explored the interplay between polyamines and colicin E7 and saw how proteins and small molecules work together with remarkable precision to sustain life2.
A turning point came during my postdoctoral work with Prof. Shuyi Zhang when my research shifted to bat hibernation and evolution3. One project revealed that the control of hibernation lies in the brain4. Another, through comparative evolutionary analyses, showed that CDH11 has been strikingly conserved across many species. Though independent, these discoveries converged in my mind and led me toward brain science.
Complexity comes in many forms. Microbes with their diversity and specialized functions form intricate universes of their own. The brain must coordinate a vast network of regions, circuits, and cell types, each communicating through delicate changes in membrane potential. Faced with the “neural traffic jams” that appear in autism I found my compass in Prof. Xiao-Bing Yuan’s course on brain development, which became a guiding star through the labyrinth of autism pathology.
Why CDH11? About 930,000 years ago human ancestors endured a severe population bottleneck, yet their brain volume expanded by roughly 43 percent4. Across nearly 200 species and a panel of cadherin genes, CDH11 stood out as the most conserved. In mouse models, loss of CDH11 disrupted presynaptic vesicle trafficking and altered neuronal activity, offering a mechanism for the repetitive behaviors seen in autism5.
Now, with our findings published in Molecular Psychiatry5, Monod’s words resonate more deeply than ever: from microbes to minds, life speaks a common molecular language. This time, molecules shape minds, and the fireworks in the neural cosmos have only just begun.
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