Welcome back from the fall vacation break. Did you ever wonder how a leaf becomes its leaf form? Jiyan Qi et al (2017) had this question and wrote a paper about it. We know that a leaf is constructed by different tissues/parts: because of differences in gene expression the upper side (adaxial domain) looks different from the lower side (abaxial domain). But which mechanism creates the flat leaf form with upper and lower side? The bud… ergo the start of a developing leaf… is round! Jiyan Qi et al (2017) showed that “relatively simple changes in mechanical properties can account for dynamic shape changes during asymmetric leaf development”. To make a long story short: In the developing (round) leaf the lower side has a higher auxin concentration as the upper side. Auxin is a plant hormone and can lead for example to cell wall loosening by de-methyl-esterification of pectins, a major component of the primary cell wall. The lower sider gets more elastic as the upper side. This difference in elasticity leads to the leaf asymmetry. With proceeding development, the rigid zone of the upper side moves to the middle. “From a physical perspective, the stiff cells receive stronger constraints from their neighbouring […] cells, such that they prefer to grow and divide by pressing on the soft inner cells“. The leaf stretches and gets flat. Just as side note: What I like about the paper is that they use computational models to test their hypothesis if differences in cell wall stiffness and epidermal restriction can lead to the leaf asymmetry. They model what would happen if the cell wall elasticity of the upper and lower region is changed/mixed up. Then they test the model predictions by manipulating the cell wall plasticity experimentally.
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Isn’t it great to know that at least half of your genome is a winner? This part of you won the race of the sperm to the egg cell. Regarding the genetic/epigenetic variation among the sperm of your father, this part of you was the fastest and robustest your father could produce. The question is, if this race between the haploid sperms of the same man, results in a sort of selection which is important for the Darwinian fitness. In other words: Does Darwin’s “The survival of the fittest” describe not only the selection among the diploid organisms but also the selection among the haploid sperm? And does this selection between the gamete phenotypes of the same man have a fitness consequence for the created offspring? Ghazal Alavioon et al. say “yes”. They selected zebrafish sperm for their longevity, and indeed, the offspring of this longevity sperm had a better survival rate and the sons which were created by longevity sperm produced significantly faster-swimming sperm compared to the sons of short living sperm. Also the fitness of the fertilized egg cell seems enhanced with longevity sperm compared to short living sperm. This fitness effect was still valid in the second generation. "Haploid selection within a single ejaculate increases offspring fitness."
Ghazal Alavioon, et al. Proceedings of the National Academy of Sciences(2017): 201705601. As you may now, biological cells consist of a variety of “walls” (membranes) which form the outer borders and separate internal compartments (“rooms” for energy production, reproduction, transport,…). In these walls there are “doors”/tunnels (channels, pumps,…) which allow molecules to pass through. However, in order to guarantee the function of the cell, it is important to control the flux of molecules and therefore many tunnels are selective for a certain type of molecules. Meaning: just certain molecules can cross through the tunnel and other molecules can not. How is this achieved? Even if there is just the right molecule around, the probability of that molecule to find this tunnel by random motion is quite low. However, in the biological cell there are thousands of different types of molecules. So the probability of the tunnel to “find” the right molecule and let it pass to the other side of the “wall” should be even lower. No! Anton Zilman et al. (2010) found out (with the help of a theoretical model and proved by experiments) that the transport probability of the tunnel-specific molecules can actually increase in the presence of non-specific molecules. To understand this, it is important to remember that the molecules move random. Inside the tunnel they may attach to it which allows them to “stay in place” for a short time, but every molecule will move at sometime in a random direction. Therefore, entering the tunnel doesn’t mean that the molecule will “walk” through the tunnel and left it on the other side of the “wall”. Another important point is that the space in the tunnel is limited. Meaning, every “spot” in the tunnel just has space for a fixed number of molecules attaching to it. The point with the selectivity is then controlled by the difference in how long a molecule can attach to the tunnel. So tunnel-specific molecules can attach longer and so can “stay” longer in the tunnel before they move randomly compared to non-specific molecules. Anton Zilman et al. (2010) created a model for the tunnel and simulated the movements of two competing molecule types (one better attaching to the tunnel than the other). The tunnel itself was divided in “spots”… so a longer tunnel has more “spots” a molecule has to cross on its way than a short tunnel. A molecule just moves to a neighboring spot when there is a free place (as said before, the “diameter” of the tunnel restricts how many molecules can be on the same place at the same time). The better attaching moecules can stay longer on a spot than then non-specific molecules. So what is happening: If the non-specific molecules have a really short attaching time, because the binding between molecule and tunnel is weak, then it does not affect the transport of the strong binding (long attaching) molecules because it has already problems to reach the entrance. In the other hand, when both molecules have strong binding, the “wrong” (non-specific) molecule can block the entrance and the transport of the specific molecule is decreased. However, if the non-specific molecule has an intermediate attaching time, it can enhance the transport of the specific molecule. The intermediate binding strength allows the non-specific molecules to enter the entrance. This hinders the return of the specific molecules which are already in the channel and so the latter “has to” go in the right direction and cross the tunnel instead of going backwards. A little bit counter intuitive, isn’t it? Just imagine there is a real tunnel and there are two types of people: one type is really fascinated by tunnel walls. They love to look at it in detail and so spend a lot of time in the tunnel while walking slowly in a random direction (because they are so distracted that they don’t know in which direction they are walking). Now you add a second type of people: people which are not afraid of tunnels and are curious but they are not so fascinated and so are moving much faster and defer to the type one people regarding a spot in the tunnel. The fascinated people will go deep in the tunnel while the hectic people stay near the entrance. The hectic people in the entrance do not hinder the fascinated people to enter the tunnel. However, as the hectic people are crowding the entrance, it is much easier for the fascinated people to walk through the tunnel instead of returning to the entrance. Therefore, more fascinated people are walking through the tunnel as it would be without the hectic people. Enhancement of Transport Selectivity through Nano-Channels by Non-Specific Competition
Anton Zilman et al. PLoS Comput Biol 6.6 (2010): e1000804. |
IdeaI love to increase my general science knowledge by reading papers from different fields of science. Here I share some of them. Archiv
März 2018
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