How Loss of Arabinoside Transferase Leads to Tomato Fascia

Topics: Stem CellsStudy

Stem cells are a class of undifferentiated cells, which differentiate to give to other cells. Every individual has stem cells in their body which the body uses as it needs it. These stem cells could be used to cure diseases. Even plants have these stem cells that are mainly located in their meristem. In recent years, researchers have taken a closer look at how the complexity of these stem cells could manipulate what gene signaling pathway plays a role in stem cell proliferation.

Recent research by Cao Xu et al has produced a major breakthrough in uncovering how arabinosyltransferases control the shoot meristem size in tomatoes. This has been seen in a very known model organism, Arabidopsis thaliana. In the paper by Xu et al, they utilized the WUS and CLV gene-signaling pathway in order to monitor the meristem size. They made a few conclusions. First, in presence of the arabinosyltransferase genes, tomato inflorescence branching mutants that had extra flowers and fruits due to enlarged meristems were defective.

Secondly, majority of the extreme mutants could be rescued with arabinosylated CLV3 but were disrupted in a hydroxyproline O-arabiosyltransferase. However, weaker mutants were defective in arabinosyltransferases indicating the full arabinosylation of CLV3 in order to maintain the meristem size. It was very interesting how they applied the study on Arabidopsis to tomatoes. They found that the fin mutants produced more inflorescence branching than fab mutants when compared to the wild type in tomatoes. In order to understand the overproliferation in fin mutants, they grew seedlings in liquid culture with low concentrations of peptides, SlCLV3 and SlCLE9 to see if the loss of arabinosylation rescued the meristems.

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They found a reduction in meristem size with its effect being greater in SlCLV3. Even with mixing equal concentrations of SlCLV3 and SlCLE9, the size of meristem was similar to wild type. This suggested that SlCLE9 played a role in the CLV signaling pathway. A break in the CLV-WUS pathway not allowing for the formation of abynosylated CLE peptides resulted in the cell overproliferation in the meristems. Also, in comparison to fin, fab2 lead to a higher proliferation of the meristems.

CRISPR/cas9 is a beneficial genome editing technique first found in bacteria and is becoming popular day by day. In this study, they utilized this system to understand fasciation caused in tomatoes due to loss of arabinosyltransferase. They mutated the closest homolog of RRA3 using CRISP/cas9 and identified RRA genes similar to RRA3 in tomatoes that encoded a predicted transmembrane domain. Using qRT-PCR, they found the expression levels to be upregulated for all SlCLV3, SlCLE9 and SlWUS. Hence, in addition to fin and fab2, they found RRA3a also function in the tomato CLV pathway. These two experiments show us the importance of the arabinosyltransferase cascade. The loss of this cascade is the determining factor of fasciation and overproliferation of meristem in the tomatoes. The author has utilized multiple techniques to show this. It is interesting to see how the size of the shoot meristem can be manipulated. If this is possible in tomatoes, I wonder if some other plants containing the CLV3 go through a similar mechanism and if they can play a role in curing any plant disease.

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How Loss of Arabinoside Transferase Leads to Tomato Fascia. (2021, Dec 23). Retrieved from https://paperap.com/how-loss-of-arabinoside-transferase-leads-to-tomato-fascia/

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