AP Biology class blog for discussing current research in Biology

Tag: cell movement

Individual Cells Move Differently When They Are Together

In a groundbreaking study, researchers have unveiled that a protein crucial for powering movement in individual cells operates distinctly when cells collaborate in groups. Cells engage in intricate pushing and pulling interactions with each other and surrounding tissues during processes such as embryonic organ formation, wound healing, pathogen pursuit, and cancer dissemination. The investigation, led by researchers at NYU Grossman School of Medicine, focused on a cluster of 140 cells known as the primordium, observing how these cells generate forces while adhering to each other during movement in zebrafish embryos—a model organism highly valued for its transparency and shared cellular mechanisms with humans.

The study reveals the role of a protein called RhoA, a primary structured protein, in propelling the group forward during embryonic development. As cells strive to move, they extend protrusions and utilize them to anchor onto nearby tissues before retracting them, a process analogized to the casting out and hauling in of an anchor.

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In AP Biology, delving into the intricacies of the RhoA protein offers a compelling view of the relationship between structure and function in molecular biology. The distinct domains within RhoA, such as the GTPase domain, Switch I and II regions, insert region, and C-terminal hypervariable region, serve as structural modules that underpin its role as a molecular switch in cellular signaling. The GTPase domain’s proficiency in binding and hydrolyzing GTP is pivotal, causing RhoA’s influence on the cytoskeleton and, consequently, cellular processes like shape modulation, adhesion, and motility. The activation and inactivation, regulated by proteins like guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs), displays these cell signaling pathways. RhoA’s dysregulation is a key player in diseases, displaying its integral contribution to maintaining cellular homeostasis. RhoA protein is a monomeric protein, meaning it does not have a quaternary structure.

Senior study author Holger Knaut, PhD, an associate professor in the Department of Cell Biology at NYU Langone Health, expressed surprise at the finding, stating, “This finding surprised us because we had no reason to suspect that the RhoA machinery required to move groups of cells would be different from that used by single cells.”

Prior research had indicated that single cells move forward by activating RhoA at their rear ends, initiating a process involving the motor protein non-muscle myosin II, resulting in cell constriction and detachment from the underlying surface.

Contrary to this, the current study revealed that cells in the primordium activate RhoA in pulses at the front of the cells, where it performs a dual role. At the front tip, RhoA stimulates the outward growth of the cell skeleton (actin meshwork), forming protrusions that grip the surface. Simultaneously, at the base of these protrusions, RhoA triggers non-muscle myosin II to pull on the actin meshwork, retracting the protrusions. This coordinated action propels the cell group forward, akin to the movement of a banana slug along the ground.

Dr. Knaut emphasized, “Our findings suggest that RhoA-induced actin flow on the basal sides of cells constitutes the motor that pulls the primordium forward, a scenario that likely underlies the movement of many cell groups.” He added that while the machinery suggests similarities in the movement of single cells and cell groups, RhoA contributes differently in each case.

Dr. Knaut also noted that a deeper understanding of the mechanisms by which cell groups move holds potential in halting the spread of cancer. He remarked, “The machinery suggests that the movement of single cells and groups of cells is similar, but that RhoA contributes to that machinery differently in each case. Within moving cell groups, RhoA generates actin flow directed toward the rear to propel the group forward.” The study’s findings could guide the design of treatments aiming to block the action of proteins implicated in the spread of cancer.

I personally never knew, especially before taking AP Biology, that cells move together. I did know that they always work together, but not necessarily that they coordinate their movements as a collective entity. It’s fascinating to learn about the intricate processes that govern cellular behavior.

I’ve been particularly intrigued by the role of proteins in these cellular functions. For instance, considering the RhoA protein, what would happen if it misfolded or denatured within our bodies? How would our body react to such a disruption? My assumption is that the consequences could be severe, possibly even leading to a breakdown in essential cellular activities. Could it be so detrimental that it might result in death? I’m curious to hear your thoughts on this matter.

I’ve been contemplating the impact of extreme heat on protein structure. If the RhoA protein were to misfold or denature due to high temperatures, it seems logical that our cells might struggle to move effectively within the body. The idea that external factors like heat could influence such fundamental cellular processes is both intriguing and concerning.

I’m curious about the specific gene responsible for coding the RhoA protein. Are there any specific diseases associated with mutations in this gene? It seems like understanding the genetic aspect could provide further insights into potential health implications.



How Did Our Baby Learn That Word?!?!

Jason Sudeikis’ character is hosting a nice dinner party with his wife played by Jennifer Aniston, and all seems to be going great. Then, all of a sudden, their 12- month-old baby blurts out a curse word! “How could our baby learn such a thing?” In a flashback 8 months earlier, we see the less-experienced parenting pair blurt out some pretty R-rated things in a fit of frustration on the road with their baby in the backseat. And so the punch line sinks in.

In modern day parenting comedies, scenes like this fabricated one are a dime a dozen. But these humorous takes on life always get at least one thing right: babies are sponges. Let’s take a look at why on a cellular level.

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Prior to birth, most neurons migrate to the frontal lobe of the brain where, during postnatal development, they link together and forge connections, allowing a baby to learn proper responses to stimuli. The “circuits” formed by the neural connections are incredibly flexible during the early months of development (roughly the first 6 months) and can quickly be formed or severed, resulting in a remarkable neonatal human ability to rapidly pick up new knowledge about our surroundings. But how are they so malleable?!

Researchers at the University of California, San Francisco may have the answer! In a study coauthored by neuropathologist Eric Huang, they found neurons forming a chain moving towards the frontal lobe from the sub ventricular zone, a layer inside the brain where nerve cells are formed, in infants up to 7 months old!

This research seems to point to the idea that these new brain cells form connections with the pre-existing neurons in the frontal lobe later in the infant’s development, resulting in more cognitive flexibility for a longer period of time.

To quote the original article by Laurel Hamers, what the new neurons are doing is analogous to “replenishing the frontal lobe’s supply of building blocks midway through construction”.

Huang’s team observed postmortem infant brain tissue under an electron microscope and discovered a group of neurons synthesizing migration proteins, but the real major discovery came with the observation of rare tissue acquired moments after death. The team injected viruses tagged with glowing proteins into the neurons (thus making the nerve cells glow) in the sample and tracked their movement. While infants up to 7 months old were observed with migrating neurons, the researchers recorded the number of migrating cells at its highest at 1.5 months old and saw it diminish thereafter. The migrating neurons usually become inhibitory interneurons which, to quote the original article, are “like stoplights for other neurons, keeping signaling in check”.

So there you have it! To make sure your baby doesn’t learn that bad word, just suck up all the migrating neurons from its brain!

All jokes aside, this research presents an amazing window into the brain development of the most intelligent species on earth! It’s fascinating how it breaks down psychological mysteries using cellular evidence. And it raises new questions about these mobile neurons: When are they created and how long does it take them to move to the frontal lobe?

How do you think this new research will influence our understanding of the creation of social biases? Do you think this will lead to breakthroughs in research on the foundation of Autism spectrum disorders?  Do you have any funny baby stories? Let me know in the comments.

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