Apical dominance, MAX and my project

One of the most important things the plant hormone auxin does is play an important role in is apical dominance. This is where the Shoot Apical Meristem (SAM), the growing part of the above ground half of the plant, produces a signal that inhibits growth from other auxiliary meristems. The SAM and auxiliary meristems contain the plant’s ‘stem cells’ and generate new leaves, stems and flowers. They both have the same ability to generate new organs. When the plant grows and leaves emerge from the meristem, an auxiliary meristem is left behind with the leaf, which may or may not grow out, just above where the leaf meets the stem. For years it was known auxin from the SAM inhibited their outgrowth. Auxin is produced in the SAM and moved down the plant and when it is stopped, the auxiliary meristem can grow out. The best person to tell you this is a gardener. When pruning, they remove the SAM on a plant, like a rose bush, to allow dormant growing parts of the plant grow out and make it bushier. It is also a pain for, let’s say for example, tobacco farmers. They ‘top’ tobacco plants so it does not grow up and make the leaves fatter. However, this stops auxin travelling down the stem and auxiliary meristems grow out. The addition of unpleasant chemicals is used to solve this problem.



Auxin does not travel up into the auxiliary meristem, so how does auxin inhibit bud outgrowth? A second signal must be involved. This ‘second messenger’ is not an easy thing to understand. It turns out to be a complex interplay of plant hormones that I will try to explain now control bud outgrowth. I will start by explaining the players involved. The hormone cytokinin (Ck) often plays the opposite role to auxin in plant grow. When it is applied to an auxiliary meristem it will grow out. Ck is generated both in the roots and locally in the stem but it is unclear which is more relevant to shoot branching (I think it varies from species to species). The auxin signalling pathway does regulate Ck synthesis but this is not the whole story. Auxin signalling pathway mutants do show some increase in shoot branching but it is lower than those affected by mutations in MAX genes (see below) and the effects of these are additive to auxin signalling.


Mutant screens reviled the MAX genes. max mutants have increased shoot branching. To cut a long story short, the MAX pathway does not produce the inhibitory signal but helps auxin regulate shoot-branching. MAX3 and 4 produce enzymes that alter a caratinoid. MAX1 is a P450 that acts downstream of MAX3 and 4 and alters the chemical further, producing the MAX-dependent hormone (more on the identity below). MAX2 does not produce the graft-transmissible signal but helps perceives the MAX-dependent hormone. In fact, it is an F-box protein like TIR1 from my post on auxin signalling. However, I think it is unlikely to bind the MAX-dependent hormone directly as TIR1 does auxin. I suppose this cannot be looked at until the hormone has been characterised better. MAX2 is also involved with leaf senescence and some features of light perception but its roles in these are not very well understood either.

The Leyser lab has been working on finding the identity of the MAX-dependent hormone but two papers published in the same September issue of Nature (just after my subscription ended!) suggest the identity in pea and rice. Ottoline has just written a short review on them (below). They found a chemical, called strigolactones, was involved. Previously shown to be involved with germination, formation of mycorrhiza with fungi and growth of parasitic plants, now it appears they are a key regulator of shoot branching. The exact identity of the biological active strigolactone is still yet to be found.

The MAX pathway’s mode of action is through limiting auxin transport. This work was published with a PhD student at York as the lead author in the Leyser lab (he was a very well known blue coat). Auxin is transported from the SAM to the roots. To move in and out of cells, auxin needs proteins to transport it. One important class are the PIN proteins. They can become localised to a particular part in a plant cell, such as the basal side, to ensure auxin only moves in one direction. This is very important in creating a vascular system in the plant. First of all, auxin is made by the auxiliary meristems but it is their ability to transport auxin out that allows them to grow out. It is best to imagine the auxin transport network as roads. Auxin (the cars) leaves the SAM and moves down the stem via PIN proteins (lanes on a motor way). In a normal plant, not all lanes are open. So auxin from the SAM fills most of the PIN proteins and only a little auxin from the buds can enter, letting some grow out. max mutants have an increase transport capacity because more PIN proteins are present. This is like opening extra lanes on a motor way so auxin from all the buds can enter and move freely, letting them grow out! Integrating the actions of all hormones leads to something like this: auxin moves down the plant and its movement down is limited by the MAX-dependent hormone from the roots. This limits the amount of auxin auxiliary merisetems can transport out, so large amounts of auxin accumulate in these buds. This (somehow) inhibits Ck production to limit growth of the bud. The integration of multiple hormones has been described as the brain of plants.

The reason max mutants and auxin signalling double mutants have an additive effect is because auxin works both through its classical signalling pathway but also through auxin transport. This is where, for me, things get confusing. How does auxin in the bud know not to be exported and form vascular tissue to connect to the main flow in the stem? This has been a long standing question, not for shoot branching but for the formation of a vascular network, yet there is no answer (or good one at least).

My final year project is in the Leyser lab, for what I hope are obvious reasons now. They have done lots of great work. A modifier of the max1 phenotype was found in a mutants screen and mapped to a location on chromosome 1. My job is to widdle the candidate genes down from around 20 to one! I don’t want to give too much away about the project on here but the mutation alters the max1 phenotype and has its own slight developmental phenotype. Hopefully understanding it will help in the long term goal of understanding plant development. I doubt it will have a direct role synthesis or degradation of the MAX-dependent hormone but I believe it will affect downstream events. I hope this has been enlighting.

Here is a very good review and explains these things better than I can do by someone in the Leyser lab:
http://www.ncbi.nlm.nih.gov/pubmed/17728300?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Here is an ahead of print short review on the identity of the MAX-dependent hormone by Ottoline:
http://www.ncbi.nlm.nih.gov/pubmed/18804430?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum