I regularly have conversations about science communication with all types of scientists and communicators in the Bay Area. One topic that frequently comes up – many of us started doing SciComm in graduate student groups. We often end up wondering – How common are science communication student groups?
To get a partial answer to that question, I started this thread asking science Twitter to respond with links to SciComm student groups:
The response was fantastic! I’ve compiled the responses in the table below (also in this google sheet). I’ll be using this list to help promote/share communication resources (particularly some from Picture as Portal). I haven’t done additional work to expand the list yet, but I will in the future. I’m also happy to add any other groups/resources you know of. Please DM me on Twitter if you’d like me to add something :D.
This post was contributed by guest blogger Jennifer Tsang, the science communications and marketing coordinator at Addgene and a freelance science writer.
A tree has a lot more going on than what meets the eye. As its leaves grow and fall, its metabolism changes, and the tree undergoes an internal overhaul. Somehow trees know exactly when these things need to happen and, each year, they happen at approximately the same time. This is a marvel of synchronization – both at the level of the trees themselves and across an individual tree’s cells. How do trees achieve this synchronization? And what are trees doing in the “in between” times of summer and winter, times when it’s hard to see much surface-level change?
Answering these questions may help us understand how trees and other plants will react to the seasons in a changing climate. Maybe we’ll even be able to work with our arboreal partners to adapt to a warming world.
Spring forward
Let’s begin with spring, the season when it seems that all life wakes up and makes an appearance: birds, flowers, even humans. For trees, spring is the time to start sprouting leaves. But how do trees know when to unfurl their foliage? For many trees, this decision depends on both day length and temperature. Trees can “see” day length using photoreceptors, sensors in their buds and on their trunks. Daylight of a certain duration signals the trees to begin budding.
Once leaves have sprouted, trees are prepared to soak up the summer sun. Leaves are chock full of chlorophyll, a green pigment that, along with sunlight, helps trees produce the sugars they need to grow. Trees spend spring and parts of summer using their leaves to generate sugars. These sugars are stored and used for energy. Before trees hunker down for winter, they also produce buds in preparation for the next year. They do so even before their current leaves fall.
Summer slowdown
As the end of summer approaches, some trees such as wild cherries slow down photosynthesis even though the sunny days continue Remember, trees produce sugars through photosynthesis. They need room to store all that sugar but have limited storage space. Thus, they slow down photosynthesis as storage space fills up. Larger trees, however, have more room for storage and will carry out photosynthesis right up to the first frost. Even in the summer, the trees know: Winter is coming.
Fall for falling leaves
Autumn’s signature explosion of color is a result of winter preparation and resource conservation. During this time, trees break down chlorophyll and store its components until spring when they can send them back out to new leaves. Without the green pigments of chlorophyll that dominate leaves in summertime, the reds, oranges, and yellows start to come out. These colors come from other pigments such as carotenes and xanthophylls. (Fun fact: carotenes and xanthophylls make carrots orange).
Cross-section of a leaf changing colors. Pigments such as chlorophyll, carotenes, and anthocyanins give us wonderful fall colors. Figure source: wikipedia.
Just as leaf growth depends on temperature and day length, trees look to these signals to decide when to shed their leaves. Contrary to what we may think, dropping leaves is actually an active process: trees grow layers of cells that sever leaves from their branches. Thus, the leaves fall with even a light breeze.
Winter hibernation
Trees shutdown many of their biological processes during winter. As part of the shutdown, trees dehydrate themselves. Freezing water expands and if a tree is too wet in the winter, it can burst. As such, some trees even begin cutting back water intake as early as July. Cells that make up leaves also hold water, so they would rupture in the winters if they didn’t fall off. Such ruptured leaves would be useless for photosynthesis.
There’s actually another important reason why leaves fall: snow is heavy. If it accumulates on leaves, it could cause trees to bend over and break. Without leaves, trees are also less susceptible to high winds during storms.
Mixed signals: changing climate against steady daylight patterns
Changes in temperature can also mean trees begin budding leaves at the wrong times. They might waste energy growing new leaves before it’s consistently warm and sunny enough for them to photosynthesize effectively. The end result: a mixed bag. Some trees might thrive in warmer temperatures while others will be woefully unprepared.
Thus the changing climate will likely shift the distribution and diversity of tree species in nature. It’s unclear what the ultimate effects of these changes will be, but other species are sure to notice the changes in the trees. After all, we depend on trees for food, building supplies, medicines, and much more. Let hope we can find new ways to protect our arboreal friends and their beautifully complex lives!
Jennifer Tsang is the science communications and marketing coordinator at Addgene and a freelance science writer. She has completed a Ph.D. in microbiology studying bacterial motility and studied antimicrobial resistance as a postdoctoral fellow. She writes for her own microbiology blog called The Microbial Menagerie. You can follow her on Twitter (@jw_tsang).
This is the first in a series of posts/videos about “model organisms.” The videos will be available here as well as on my Instagram account.
Researchers, like most people, have limited time and space. Thus, when setting up experiments, they often try to do so in the most efficient, practical and informative ways possible. This leads many scientists to work with so-called “model organisms.” Model organisms are living things that are particularly easy to work with in the lab. They often grow quickly, are small, and are easy to care for.
Scientists use different model organisms to study different processes. They do so in the hopes that what they learn from these models will be applicable to other living things. This doesn’t always turn out to be true, but, with the right model organisms, scientists can learn a lot.
As you can see below, I’ll be drawing top hats on all my depictions of model organisms. The top hats symbolize that, in many ways, model organisms are going out of style. This is because new biotech tools (eg. CRISPR) make it easier to work with all sorts of organisms. Model organisms just aren’t as necessary as they used to be. Nonetheless, we have learned a lot from these models and we’re sure to learn a lot more from them in the future.
Axolotl: A great model organism for regenerative biology, stem cell, and developmental research
Our first model organism (pictured here) is type of salamander known as an axolotl.
Axolotl are particularly useful to biologists studying stem cells and regeneration. This is because they’re crazzzzy good at regrowing their body parts. In fact, you can cut off a whole axolotl limb and it will grow back!
This amazing ability also makes axolotl great tools for studying developmental biology. This field focuses on the processes by which animals form complex tissues, organs, and whole bodies.
For example, by monitoring axolotl as they regrow body parts, we learn how their cells coordinate with one another. Cells may use similar coordination mechanisms during human development. Thus working with axolotl can provide insights into our own biology!
That’s it for now, more model organism posts to come!
Note from Tyler – I’ve been stretched a little too thin to update this blog as much as I’d like. However, I’m always down to help scientists edit stories about their own work and feature them here as guest blog posts! Below you’ll find my first guest blog post from Danny Ward, a PhD student at the John Innes Centre. If you’d like to write a story about your own work and feature it here, please reach out! Without further ado, I’ll let Danny Ward introduce himself.
My name is Danny Ward and I am a PhD student who works in a laboratory. I carry out experiments in the research field of molecular microbiology. This means I look at the tiny bits inside microscopic creatures to understand more about how they work.
Micro-organisms, tiny living things, are all around us. Some are beneficial to us. For example, we use them to make foods (like cheese and yoghurt) and medicines (like antibiotics). Others can be very bad for us. They can make us sick and cause disease. Many can be treated with some bedrest, while others can be life threatening!
I work on bacteria, a type of micro-organism. In particular, I study disease-causing bacteria called pseudomonas. These bacteria can infect animals, plants and us humans!
I study pseudomonas through the lens of molecular microbiology. In this field we study how micro-organisms work at the subcellular level. I look inside individual bacterial cells to understand how teeny tiny biological molecules like proteins and DNA interact with one another to give Pseudomonas life.
This is a fascinatingly complex area which we still don’t fully understand. We don’t know how all these biological molecules work, how they came to be, how we can control them, and how we can use them for good. Understanding more about microbiology can lead to new knowledge, medical advances, and biotechnological products. As you’ll learn below, my work might help us create new antibiotics!
Attacking cells with tiny biological needles
I specifically study how pseudomonas infect cells. During infection, pseudomonas attack cells using tiny biological needles. Scientists call these needles “type III secretion systems.” With the power of microscopic motors behind them, these needles inject nasty proteins into cells. The proteins enable pseudomonas to colonize their hosts and cause disease.
Pseudomonas and their type III secretion systems. A) A petri dish with pseudomonas bacteria. B) Close up diagram showing a single pseudomonas cell with its type III secretion systems (infectious needles) in pink. C) Close up diagram showing a single pseudomonas cell using its type III secretion system to infect a plant cell.
We don’t completely understand how the needles work. We know what they do but we lack detailed understanding. For example, we don’t know how pseudomonas control their needles. The needles need a lot of energy and resources to operate. Thus it’s advantageous for pseudomonas to precisely control them. The pseudomonas only spend the energy necessary to operate their needles when there are cells for them to infect.
Indeed, figuring out how pseudomonas and other bacteria control similar needles has potential health applications. We might be able to exploit this information to control the needles ourselves. Thus, we could potentially control infection and stop the spread of disease.
Controlling type III secretion systems
Pseudomonas control their needles with “signalling molecules.” These are biological compounds that alter cellular processes. Like traffic signals, signalling molecules can turn process on, off, slow them down, or even speed them up. Usually cellular signalling molecules take the form of chemicals. These attach to different parts of cells to speed up or slow down processes. Often they bind to proteins on the surface of cells called “receptors“
In Pseudomonas, an important signalling molecule is known as cyclic-di-GMP or CdG for short. After many experiments, we’ve learned that CdG controls the pseudomonas type III secretion system. Now I’m trying to figure out how CdG exerts its control. This means a lot more experiments at the laboratory bench! For example, I’m looking to see if the CdG molecule binds to proteins found in the type III secretion system. I’m also doing experiments to see if CdG speeds up or slows down the tiny motors that power the needles.
With this information, we may be able to develop new ways to slow down or disable Type III secretion systems. We could potentially use this knowledge to keep pseudomonas and similar types of bacteria from causing disease. For example we could search for chemicals that prevent the CdG signalling molecule from interacting with the needle. These chemicals could be the basis for future drugs that treat infection! This is a great thing because many bacteria have grown resistant to the common antibiotics used today.
This PhD is being funded by “the UKRI Biotechnology and Biological Sciences Research Council Norwich Research Park Biosciences Doctoral Training Partnership”.
This article was written by Danny Ward, a molecular microbiology PhD student from Norwich, England.
I’ll write a regular blog post some time soon, but hey, these expanded instagram stories are basically like 3 quick blog posts. Enjoy!
Butterfly diversity
Moths and butterflies together form a group of animals known as Lepidoptera. There are apparently nearly 180,000 known species of them. I stumbled across this somewhat mind-boggling fact while reading butterfly research paper. In the paper, researchers used a genetic engineering technique to break a butterfly gene. This particular gene affects butterfly wing patterns. By breaking it, researchers changed butterfly wing patterns. Indeed, breaking the gene in different butterfly species resulted in different patterns. Thus, this single gene had different roles in different species. This is cool because it shows how adaptable genes are. It also reminds us that animal development in complicated!
Animal cloning for livestock breeding
Animal cloning is the process by which scientists take genetic material from one animal and use it to create new animals. As a result, the new animals are, more or less, copies of the original. You might remember when scientists cloned Dolly the sheep back in 1996. This probably seemed like a simple curiosity back then. Yet, farmers regularly use cloning techniques now. With cloning, they can speed up the process of breeding new livestock with desirable genetic traits like increased muscle mass or milk production. Once they have one animal with the right mix of traits, they can clone this animal. The clones can then breed with many other animals. Thus, the clones quickly spread their beneficial traits throughout the herd.
Viruses infect plants
Plants, just like animals, get sick. Indeed, they can be infected with viruses. Such viruses can can kill crops and are huge problems for farmers. Scientists hope to use genetic engineering techniques to make crops resistant to viruses. Indeed, they used such techniques to save Hawaii’s rainbow Papaya back in the 90s. Modern genetic engineering techniques are easier to use than those from the 90s. They will hopefully save even more crops!
Here’s a round-up of some of the stories from my SciCommByTyler instagram account. Follow me on instagram to see similar stories each weekday!
Pig sperm don’t freeze well
Many farmers use artificial insemination to breed their animals. This process involves injecting female animals with sperm from specific males. With artificial insemination, farmers can quickly breed their best male animals with many females. The result is many offspring with useful traits.
It is useful to be able to freeze sperm from high quality males. Such frozen sperm can be transported to other farms or stored for future use. This helps spread useful genetic traits.
Unfortunately, farmers don’t have super effective ways to freeze pig sperm. Many pig sperm die during the freezing process. Farmers still use artificial insemination for pig breeding. It’s just more difficult to store or transport pig sperm for extended use.
Like all organisms, trees have DNA. Specific kinds of trees have specific DNA sequences that give them particular qualities. Natural forests are composed of many different trees with different DNA sequences. They are beautifully diverse jumbles.
In contrast, tree farmers often grow rows and rows of trees with identical DNA – tree clones. They do so because they want many trees with very specific characteristics. These characteristics make their wood valuable for particular uses. Clonal forests are beautiful in their own way.
Injecting viruses into the eye
DNA sequences encode cellular parts that give cells their functions. In some forms of blindness, altered DNA sequences encode broken parts. These broken parts can lead to progressive vision loss.
It’s hard to get such viruses to some parts of the body. However, it’s actually quite easy to get them into the eye. Thus scientists can inject viruses with corrective DNA sequences into the eye and restore vision to some patients.
I often come across interesting biology facts. I spam these facts in polite conversation, but I’ve also decided to share them in a more productive way on Instagram. On the SciComm By Tyler instagram account, I’ll post detailed drawings coupled to nuggets of biological intrigue. Some of these will come from blog posts. Through the stories feature, I’ll share more bite-sized biological morsels. I’ll couple the stories with goofy doodles (sometimes I’ll recycle these from my gallery :P). At the end of each week, I plan on delving into the stories in a little more detail through a blog post.
Below, I expand on my first week of stories. Enjoy!
Biosensors are biological machines that detect objects and events
I wrote a bit about biosensors in an older blog post. As a refresher, biosensors are biological machines that detect specific objects and events. They have many research uses. They can detect chemicals, they can detect organisms, and some can even count how many times cells divide.
I first became enamored with biosensors during my PhD work. For part of my work, I tried to get bacteria to turn sugar into gasoline. To see if my bacteria were accomplishing this goal, I designed a biosensor. This biosensor made the bacteria turn red if they produced gasoline-like chemicals. Indeed, the more gasoline-like chemicals they produced, the more red they’d become. Unfortunately, my biosensor wasn’t particularly sensitive so I abandoned it (such is the nature of many experimental research projects!).
Others have created more useful sensors. The doodle above illustrates a biosensor that detects DNA. Such biosensors bind to specific DNA sequences and glow. They help scientists understand how DNA sequences interact with other things in cells. Using many different biosensors, scientists learn how cells function. Scientists can then use their knowledge to create therapeutics or even design cells that do cool things like attack cancer cells!
Komodo dragons use venom to kill prey
I think Komodo dragons are super cool. Even if they don’t breathe fire, they’re still basically dragons. Long ago, I was told that Komodo dragons don’t directly kill their prey. Supposedly, they instead transferred bacteria to their pray through biting. The resulting infections then killed their prey over time. Recently, I learned that RESEARCHERS DO NOT BELIEVE THIS ANYMORE. Indeed, when I was at the San Francisco Zoo a few days ago, I read that Komodo dragon bites inject venom into their prey. This venom kills prey through a mixture of physiological effects. For instance, the venom can lower blood pressure and prevent clotting. It’s not fire, but it’s pretty brutal!
Some frogs survive being frozen
Okay, I’m a molecular and cell biologist at heart, but I love me a good animal fact! I picked this one up while watching one of the many BBC nature documentaries on Netflix. I don’t have much more information than what’s in the image. I just think it’s really cool! Hopefully, I’ll dive into this in a dedicated post at some point.
Some bacteria inject DNA into plants
Bacteria do soooooo much more than make us sick. There are many bacteria that do good things. We’ve even figured out how to turn some dangerous bacteria into useful tools. For example, there are bacteria that use teeny tiny needles to inject their DNA into plant cells. These bacteria naturally cause plant diseases. However, scientists have figured out how to use these bacteria to deliver useful DNA sequences to plants. They can even use these bacteria to make crops resistant to pests! Learn a little more about plant biotech in this post.
Complex meats are hard to make in the lab!
Many companies are working to grow meat and meat-like products in the lab. They hope to produce these “meats” more sustainably than livestock. They are having a lot of success growing meats like chicken nuggets or ground beef. However, it will be some time before we have more complicated meats like steaks or pork chops. The complex structures of these meats are difficult to create in the lab.
That’s all for this week. Please follow me on Instagram to check out my stories in real time. Cheers!
In this post from the BiLOLogy archives, I discuss why I did my PhD work on E. coli fatty acid synthesis. This post was originally published back in August 2012 – the start of my 3rd year of graduate school. Enjoy!
Why work on fatty acid synthesis? I can explain the reasoning by showing you the structure of a fatty acid (Figure 1):
Figure 1: Fatty acid (octanoate) structure
The corners connecting the black sticks in this fatty acid are carbons. The sticks themselves are bonds. All carbon atoms in any chemical compound need to be connected to other atoms by 4 bonds. NO MORE, NO LESS. The fatty acid can be broken into two regions: the fatty acid head (the part with all the O’s which are oxygens) and the tail, which consists of only carbons and hydrogens. The hydrogens are not drawn, but, if they were, the picture would look like this instead:
Figure 2: Fatty acid (octanoate) structure with all hydrogens (H’s) and carbons (C’s) labeled
Clearly, this figure is much less appealing, letters scattered all over the place and all, but we can see that all the carbon atoms have the appropriate number of bonds. The hydrogens simply aren’t drawn in the first figure.
What’s important is that all of these carbon-hydrogen bonds are full of potential energy. In fact, if we compare octane, a component of gasoline, to the fatty acid, we see that the fatty acid’s tail is nearly identical (figure 3). Indeed, through a variety of mechanisms, humans and bacteria can convert fatty acids into compounds, like octane, that can be used as fuels directly.
Figure 3: Octane structure
How can we make fatty acids? One way (though, I have to admit, not necessarily the best way right now) is to use E.coli. E.coli make fatty acids through a process that I can explain using the comic. Fatty acids, like the warrior’s sword, start out small. They begin as the two carbon compound acetyl coA.
Figure 4: Acetyl coA
E.coli (and many other organisms including you) form acetyl coA by breaking down glucose and other sugars. You can think of these sugars as the monsters (the mini-skeleton and the lizard thingy) attacked by the warrior in the comic. As bacteria break down glucose using a bunch of enzymes, they acquire energy from it. One of the products of this break-down process is acetyl coA. Acetyl coA can be used for a number of things. It can even be broken down further for more energy. Alternatively, bacteria can use some of the energy they get from glucose to combine multiple acetyl coAs to form fatty acid precursors called fatty acyl CoAs. Each acetyl coA added increases the size of the growing fatty acyl CoA by two carbon units (figure 5).
Figure 5: Adding acetyl coA onto a growing fatty acid (fatty acyl coA) increases its length by two carbons*
*Caution: Despite the stars, enzymes are not magical, they follow physical laws and simply help speed up reactions… the stars are just here to indicate that there’s more going on here than I’m letting on.
Just as the warrior uses the energy to make the sword bigger, E.coli can use acetyl CoA and the energy they get from glucose to make longer and longer fatty acids. E.coli use these different fatty acids to modulate the properties of their cell membranes (layers of molecules that separate the inside of the cell from its surroundings).
In my work, I try to direct E.coli to produce specific length fatty acids with desirable fuel properties.
Way back in 2017, I wrote a post about how scientists might one day use pigs to grow human organs. These “human-pig chimeras” could provide replacement organs to people with diseases like diabetes.
I recently learned that researchers are also trying to make pig organs suitable for transplant into humans. Their work doesn’t rely on putting human cells in pigs; they don’t need to make chimeras. Instead, these researchers use genetic engineering techniques to make pig organs more acceptable to the human body. Their modifications prevent the immune system from attacking and rejecting the pig organs. Thus, they hope to make pigs the future heroes of organ transplantation.
This research holds a lot of promise for patients in need of organs. Yet, it’s reasonable to worry that we devalue pigs by using them to produce human organs. My take is, if we accept pigs are sources of food, we should accept them as sources of organs. Nonetheless, I believe that we should develop transplant and food systems that don’t rely on living animals. Learning how to grow organs in pigs may help us move in this direction. Hopefully, we’ll eventually know enough about organ development to simply grow organs (and meat for consumption) in the lab.
One day we may be able to transplant pig pancreases (pigcreases?) like this to patients in need.
“Receptor.” It’s yet another bit of biological jargon. It sounds like receptors should be small spacecraft launched to defend an alien mothership. Or maybe receptors are courtly underlings who receive guests before their presentation to the queen? In truth, receptors are cool and important biological structures that reside on cell surfaces.
As you might remember from my post on cell membranes, the layers of fat that surround cells are quite complex. They are studded with proteins that perform many functions. Some of these proteins are receptors.
Receptors all detect stimuli and cause cells to respond in some way. Often, receptors grab onto specific molecules floating nearby. Then they signal to the cell that they’ve done so.
The exact cellular response to a receptor signal depends on the receptor and on the stimulus detected. Some signals cause cells to grow. Others cause cells to move. Still others coordinate behaviors among many cells. Receptors are critical for many of life’s complicated processes.
Unfortunately, receptors have a darker side too. Many viruses use receptors as handles. With a good hold a on receptor, a virus can barge into a cell. Thus viruses hijack receptors to infect cells and cause disease.
A virus grabbing onto a receptor to infect a cell.
Using receptor biology to prevent viral infection
Interestingly, scientists are using receptors to fight viral infections. They reason that, if they get rid of receptors used by viruses, the viruses will have no way of infecting cells. Many receptors are only important under specific circumstances. Thus, getting rid of them will have some small negative consequences, but the benefits of resisting viral infection are worth it.
Indeed, a scientist in China recently claimed to have modified babies to make them resistant to HIV (these are the so-called “CRISPR babies”). This scientist used a genetic technique to delete one of the receptors hijacked by HIV. The researcher performed this technique in embryos. Thus all the modified babies’ should be able to pass their modifications to their offspring.
What this scientist did was foolish for many reasons. Some of them include:
It is unclear if the technique was safe.
It is unclear if the technique accomplished its goal.
There are effective ways to prevent HIV transmission that don’t require this technique.
Some types of HIV use other receptors. Thus, the children won’t be protected from all types of HIV.
On top of all this, the scientist’s use of this technique raises many ethical questions. Most of these stem from the fact that the babies can pass on their human-designed modifications to their offspring. Should we modify the human gene pool in this way? Do we know enough about the potential consequences? Can we use similar techniques to do more than treat disease? Society at large must face all of these questions before we decide to use any similar techniques again.
This unfortunate work aside, other techniques modify receptors on adult cells. Future generations can’t inherit the modifications. Thus we can use these techniques following standard regulatory rules. Indeed, clinical trials using modified adult cells to treat HIV have had very promising results! Scientists can also give immune cells receptors that make them better at fighting cancer (see my previous discussion of CAR-T cells in this post). Receptors play a role in so many biological processes that we’ll likely see many more cool uses of them soon!
The next time you see a picture of smooth, round cell, remember that it’s studded with receptors and they do a lot!
