Controlling pluripotency and differentiation in plant cells: the KNOX-TCP regulatory module

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Development in multicellular organisms involves the differentiation of specific cell-, tissue- and organ-types from progenitor stem cell populations. In plants such as Arabidopsis thaliana, a commonly used model organism used in the study of plant developmental biology, pluripotent stem cells are located in a pool of undifferentiated cells termed the shoot apical meristem (SAM), which gives rise to lateral organs such as leaves. Leaf cells subsequently undergo differentiation associated with their specialised functions, such as photosynthesis and gas exchange. Numerous genes have been identified that are involved in controlling the formation and sustained function of the SAM. Some genes act to confer a state of pluripotency - that is to say, an undifferentiated state with the ability to form any type of cell - while others promote differentiation into specialised cell types. Most of the genes currently known to regulate SAM function encode a type of protein called a transcription factor (TF). TFs are proteins that regulate the expression of other so-called 'target' genes by activating or repressing their expression - specifically by controlling the transcription of a gene from DNA into RNA, which is subsequently translated into a functional protein. Of the many different types of TF that have been shown to be involved in SAM regulation, the KNOTTED1-like homeobox (KNOX) gene SHOOT MERISTEMLESS (STM) encodes a TF that is absolutely critical for the specification and maintenance of pluripotent cell fate in the SAM. My recent work has shown that STM represses the expression of a different type of TF belonging to the TCP family (TCP4), which is involved in promoting differentiation in leaves. Interestingly, TCP TFs have previously been shown to repress the expression of STM. Hence, I have revealed a mutually antagonistic relationship between these two important classes of TF: STM promotes pluripotency and represses TCP expression in the SAM, thereby preventing meristem cell differentiation, while TCP represses STM expression and promotes differentiation in developing leaves. Loss of STM function or elevated levels of TCP causes the cells of the SAM to differentiate and cease activity. Conversely, loss of TCP mimics the effect of elevated STM expression, such as inhibited leaf differentiation. Given these similarities, one might expect that STM and TCPs regulate, in an antagonistic manner, a common set of target genes that lead to cells adopting pluripotent or differentiated fates.The control of pluripotency and differentiation is the central theme of this research project. Specifically, this project seeks to understand how cell fate decisions are made in the SAM by studying the interplay between STM and TCP, identifying TCP-regulated target genes and comparing these with those previously identified for STM. Using fluorescent 'reporters' for these two genes, changes in STM and TCP expression in the living SAM will be monitored when levels of TCP or STM levels are artificially increased or decreased respectively, revealing in which cells their expression changes and the how quickly this occurs. Having previously identified the STM target genes that promote pluripotency, characterisation of TCP target genes will enable the identification of target genes that promote differentiation. Comparative analyses will reveal which genes are competitively regulated by STM and TCP. These would likely represent key players for the adoption of pluripotent or differentiated cell fates and would represent a considerable advance in our understanding of the control of pluripotency and differentiation in plant development.