The tomatoes we eat today were almost 10 times smaller years ago. So how did the size and thickness just increase over time? It was just by random chance. It is as simple as that – one day a farmer had found a tomato slight bigger than what he had been cultivating – technically an anomaly – and he grew that tomato over and over again. Domestication of tomatoes has led to us getting the fruit we take for granted so easily. The process may have been simple, but the mechanism was much more complex. The paper “A cascade of arabinosyltransferases controls shoot meristem size in tomato” (Xu, Cao, et al 2015) breaks down the mechanism through which we ended up with the mutation that gave us our tomatoes. Growing plants have shoots containing meristems which contain stem cells. Stem cells have the ability to become absolutely any cell they want. As they multiply, the meristem grows bigger and bigger, allowing more flowers and fruits etc. However, that is not what happened with these tomato plants originally. An original pathway looked something like this: a gene expressed a protein name WUSCHEL (WUS). This protein is in charge of causing the meristem to grow in size, but it also activates its repressor CLAVATA3 (CLV3). CLV3, being a ligand, attaches to the receptor protein, CLAVATA1 (CLV1). This is allows the activity of WUS to be deactivated and so the meristem cannot grow in size.
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