A recent paper in Current Biology suggests that plantscan be engineered against climate change, even drought. Researchers propose to do this by making the plants better at handling stress. Now I know what you might be thinking — ‘stress’, ‘climate change’ — it sounds like it’s time to call the plant acupuncturist. However, there is actually some fascinating new science hiding behind claims like this.
All plants need to photosynthesize to survive. But when you throw in environmental stressors like excess heat, cold, drought, salt, or herbicides, just photosynthesizing can be deadly. Even in the absence of any of these assaults, too much sun can be worse than too little. The fact that chlorophyll’s absorption spectrum makes things surprisingly green reflects the compromises inherent in being able to capture every photon possible when they are scarce, yet field only just enough when they are plentiful.
When plants are forced to photosynthesize under conditions where it would probably be better not to even bother, their chloroplasts create additional stresses all by themselves. That is to say, they they generate and leak harmful free radicals that ultimately do damage to proteins, DNA and lipids. Although they can’t just move into the shade, plants have evolved certain molecular adjustments to deal with this situation. What the researchers suggest, is that plants could be made more resistant to drought by tweaking some of these responses.
They found that increasing the levels of a protein called SP1 made plants more resistant to environmental stresses by decreasing free radical production. The simple explanation is that SP1 depletes the protein complexes that enable the double-membraned chloroplasts to import the photosynthetic machinery they need. This import complex goes by the name of TIC-TOC, for translocon at the inner, and outer chloroplast. Although chloroplasts make many of their own proteins, the nucleus contributes the bulk of what they need. Turning down TIC-TOC can therefore turn down photosynthesis when the plant detects stress.
Beneath this superficially crude mechanism lie untold layers of regulatory nuance. SP1 is actually a codeword, gene speak for ‘Ubiquitin E3 Ligase’. Ubiquitins are essentially molecular tags that are found everywhere in the cell. They can be thought of as little burrs that proteins accumulate over time as they amble about — much like a hiker accumulates various burrs when walking in the brush. When a protein has too many burrs it gets sent to the jailhouse, typically an acid-filled lysosome from which there is no escape. It’s the cell’s way of saying to the protein, ‘you’ve a had a good run, but your services will no longer be needed’.
These ubiquitin pathways evolved much in parallel to other familiar markup systems used in the cell, namely methylation of DNA, and phosphorylation of specific amino acids in proteins. As we recently saw for similar kinds of protein modifications in genetic recombination and repair, the scope of these regulatory pathways extends well beyond mere protein degradation. In fact they have a hand in nearly every aspect of cell function, and can serve in a very real sense as its pulse.
The ubiquitination system differs in one key way from the methylation and phosphorylation timing operations we mentioned above. Although these two tags toggle DNA expression and duplication, and even pace the cell cycle, they only attach at certain putative sites. On the other hand, ubiquitins have a subtle trick up their sleeves — they can tag other tags. This gives them a near-exponential flexibility, especially when compared to simple binary labels. But not only that, these linear tapes come with their own set of tinker-toy connector blocks; special ubiquitins that alow them to branch repeatedly. These generate a fractalized language all its own, one complete with an entire vocabulary of different ubiquitin subunits.
Now the ubiquitin E3 ligase itself is just one specific kind of ubiquitin ligase whose job it is to add some of these subunits together under specific cellular conditions. When you consider that the human genome codes for over 600 different forms of just the E3 ligases alone, you begin to have some appreciation for the scope and thoroughness of this controller. The researchers are fiddling here with just one of these ligases and seeing some tangible results in the plant as far as drought susceptibility.
Certainly this all is a nice a start. However, we should caution that while humans already have clear ability to modify plants for resistance against a particular parasite, or perhaps even for something like freeze tolerance, modifying them for climate change is not something we should claim (at least at this early point in the game) to be able to do any better than the plant itself might do.