Friday, July 15, 2016

Attack of the mutant thistle: homeotic genes and how a cell knows what organ to become

Over the weekend, I was looking around for some populations of Cirsium vulgare (bull thistle) for my research, and while wandering, I noticed a rather remarkable individual that displays several physiological mutations.

For context, here's a full-plant view of a reasonably normal (ie representative) individual, which was only about 2m away from our plant of interest.

Cirsium vulgare, structurally representative individual
It clearly has a central stalk from which numerous branches emerge, each topped with one to three (ish) flower buds. Most individuals were not yet actively blooming this weekend.

To understand what's going on here, some knowledge of plant development is required. This is not my area of expertise, so I apologize for any minor inaccuracies which may be found in the descriptions below.

When a plant is developing normally, the cells can be broadly split into two categories: differentiated cells, and meristematic cells. Meristematic cells are found in the areas of the plant experiencing active growth: root tips, stem tips, and flower buds. These cells have not yet become differentiated, that is to say that they are not yet assigned to a particular organ type (e.g. stem, leaf, petal, etc.). The areas where these cells are found are the places of active growth and development in a plant.

There are a regulatory genes which are responsible for determining which cells become which types of organs (they tell the meristematic cells what to become), which are broadly referred to as homeotic genes. The proper functioning of these genes is essential to the accurate physiological (anatomical) development of an organism. When homeotic genes are not functioning correctly, the consequence is usually a non-viable organism (i.e. an organism which cannot live). Sometimes, however, a mutation can occur to homeotic genes which is survivable. Generally, when something is seriously wrong with the physiology or anatomy of an organism, there's a good chance that a malfunctioning homeotic gene is responsible.

Homeotic genes are not exclusively found in kindom Plantae; indeed, quite a lot of research has been conducted on the function of homeotic genes in kingdom Animalia, especially with flies. There's quite a lot of interesting research about homeotic gene mutations or gene knockouts resulting in abnormal physiological development in many organisms, such as this study in mice which found that the silencing of one homeotic gene resulted in a continuation of anterior (front-body) anatomy development further along the body of mice -- basically, extra ribs.

A lot of studies have been conducted in this area for plants, as well, particularly using Arabidopsis thaliana, the world's most popular plant research organism. Manipulations of homeotic genes of this plant have isolated the particular genes responsible for the development of assorted organs in plants.

Now let's take a look at our unusual individual.

Whaaaaa-? Mutant C. vulgare

The most obvious oddity about this particular individual, from a distance, is the exceptionally thick stalk and lack of branching. It looks rather like a small tree from a distance (my husband mistook it for one at first).

If we get in closer, we can see that the stalk seems to be many fused stalks (note the vertical striations, and the strangely wide & flat shape). This is either because all the branching stalks have failed to separate from the trunk (possible), or because the apical meristem (developing portion of the vegetative part of the plant) is fasciated (misshapen, resulting in elongation along one plane). Hard to decide. I'm tempted to say fasciated, but the total lack of branching stems is throwing me off on that conclusion.

Close-up of the mutant C. vulgare's central stalk; note the vertical striations and odd shape
The next weird thing about this particular individual only becomes obvious once one gets in a bit closer to take a look at the top of the plant, where we expect to see flower buds. Instead of normal C. vulgare flower buds, we see this:

Huh? Flower buds of mutant C. vulgare

Cirsium vulgare flowers normally have a rather large receptacle (the lowest part of the flower, essentially a swelling of the stalk, which is often seen as a bulbous portion below the organs we more readily recognize as 'flower'), covered with spikes. In place of this spiky receptacle, this mutant individual has an abundance of leaves. When cells which should have developed into one organ instead become another, we call this homeosis.

Finally, if you look closely at the flower bud in the lower right of the above picture, you can see that it is not classically round, instead looking strangely comma-shaped. This is called floral fasciation, where the floral apical meristem (portion of the plant actively developing into floral organs) becomes misshapen, so instead of round it gets stretched out like this.

You might be wondering at this point -- is this common? Well, no, such mutations are quite rare in natural populations, although it may be more accurate to say that such mutations are rarely found in living, viable individuals in natural populations (most of the time such mutations mean that the organism is nonviable and so never grows/develops, or dies extremely young).

You may also be wondering -- how did this happen? Well, that's a bigger question. I can't establish from observation of the plant, for example, whether the problem is that the homeotic genes themselves are altered (i.e. the genetic code is wrong), or whether the homeotic genes are simply malfunctioning. The anatomical oddness of the individual could be the consequence of viral infection, fungal infection, parasitism, hormonal abnormalities, or genetic changes. Unfortunately, I don't have the tools necessary to determine how the mutant individual pictured above came about.

Given the sheer number of obvious mutations on this individual, I suspect that there is an external cause (i.e. that the mutations are induced), because this would be the simplest explanation. All the mutations being the product of a fungal, viral, or parasitic infection is a simpler scenario than the idea that each mutation has a separate cause (which would be the case if this were a product of actual genetic chances). Of course, they may also be a product of a hormonal abnormality resulting from a single genetic mutation. I have no means of determining the cause, so unfortunately my speculation will remain speculation and I shall have to leave my curiosity unsatisfied on this score.

Of course, this individual will not be used in my research. It is entirely too non-representative. Despite being unsuitable for my work, at least it was an interesting specimen!

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