Tree of the month: YODA as a (jedi) master regulator of Arabidopsis organogenesis
Luke arrived to the swamps of Dagobah looking for the other jedi master that, according to Obi Wan, will be able to train him further. Before him, however, the only being that stood was an old and senile alien goblin that liked to mess up with his electronic devices. The young apprentice had two lessons to learn from that first encounter: To control his anger and to never judge a book by its cover. After that introduction in The empire strikes back, Master Yoda became one of the most iconic characters of all the Star Wars fictional universe, a little imp that was secretly one of the greatest mystics of all the galaxy.
It has been a month since the release of The force awakens, the new Star Wars movie and first instance of a new trilogy. Many were excited to see a new entry of the saga, some others were still haunted by the force ghosts of the prequels, and many others simply do not understand all the hype. But Star Wars is an institution, and probably the single most influential piece of media ever released. And that influence is also visible in the realm of academia. Hell, even something as criticized as the midichlorians from the Phantom menace gave name to a genus of bacteria!
Naturally, a character as pivotal as the tiniest grand jedi master should have some representation in scientific literature. Thus, in the late 90’s YODA was described in a scan for development mutants of Arabidopsis thaliana. Mutants for YODA, as the one from the picture in the right, showed extreme dwarfism, infertility and a high percent of inviability when planted in soil. The gene was later identified as a member of the Mitogen Activated Kinase Kinase Kinase (MAPK3), the last component of a common signaling pathway that commonly regulates cell division and differentiation, as well as as response to hormones both in animals and plants.
But, just like the old master, the small size of the mutants was hiding an unsuspected big role in the big picture. Years later it was observed that YODA mutants affected the development of stomata, the small pores that plants use to regulate gas and water exchange, producing an overproliferation of them. Furthermore, overexpression of YODA caused the first phenotype lacking stomata ever identified, a promising trait that is shedding light to the molecular biology of these essential pores. Stomata regulate the water content of the plant and was an essential innovation that allowed plant to colonize dry land. And important as it may be, the contribution of YODA to the formation of stomata is a secondary feat. YODA de essential for the right regulation of a wide array of asymmetric cell divisions in Arabidopsis. This naturally includes the formation of the guard cells of the stomata, but also the flower organogenesis, which explains the infertility in YODA mutants; and the very first cell division in the embryo, which determines the root-shoot axis. The involvement in this last process explains the extreme dwarfism of the mutant, as the plant has impaired the most basic reference for its own body plan.
Looking at the high degree of sequence and synteny conservation of many early developmental genes in metazoa, one would be tempted to suggest a similar evolutionary pattern for YODA. However, as we can observe in our tree of the month, this is simply false. This may happen because of the highly dynamic nature of plant genomes, whose history is plagued by whole genome duplications; because of its role in the development of a highly ecology-dependent structure as the stomata; or simply because development in plants is much more flexible than in animals. Whatever the reason, the gene shows a considerable degree of duplication and paralogy in other plant species. Many other stories await in the phylome 28, Arabidopsis thaliana in the context of 20 plant species and 5 outgroups. And may the force be with you!
References:
http://www.ncbi.nlm.nih.gov/pubmed/15203025
http://www.ncbi.nlm.nih.gov/pubmed/17259259
http://www.ncbi.nlm.nih.gov/pubmed/23263767
http://www.ncbi.nlm.nih.gov/pubmed/24006425
http://www.ncbi.nlm.nih.gov/pubmed/24923680
http://www.ncbi.nlm.nih.gov/pubmed/24646252
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