Biología y Genética 🧬

5 months ago

Científicos han demostrado que la microgravedad simulada desorienta a los espermatozoides mamíferos, reduciendo su navegación hacia el óvulo y el éxito de fertilización. https://t.co/GI1K5qVqnS

BiologiaC1's tweet photo. Científicos han demostrado que la microgravedad simulada desorienta a los espermatozoides mamíferos, reduciendo su navegación hacia el óvulo y el éxito de fertilización.

https://t.co/GI1K5qVqnS https://t.co/l75OAdF5u2

5 months ago

Investigadores de París y Tokio han cifrado y descifrado en tiempo real un documento completo usando solo claves generadas a partir de ADN sintético https://t.co/z6YqcXxp0j

BiologiaC1's tweet photo. Investigadores de París y Tokio han cifrado y descifrado en tiempo real un documento completo usando solo claves generadas a partir de ADN sintético

https://t.co/z6YqcXxp0j https://t.co/SX4L5OA4w8

5 months ago

Un sistema de inteligencia artificial multiagente, es capaz de analizar síntomas complejos y datos genéticos, supera a médicos y modelos previos al reducir años de incertidumbre diagnóstica en cuestión de minutos. https://t.co/BAcSyzsxhj

BiologiaC1's tweet photo. Un sistema de inteligencia artificial multiagente, es capaz de analizar síntomas complejos y datos genéticos, supera a médicos y modelos previos al reducir años de incertidumbre diagnóstica en cuestión de minutos.

https://t.co/BAcSyzsxhj https://t.co/Xex6Jzfel6

Cosas random de naturaleza y biología. Nuestro sitio web online desde 2006. Instagram: @cienciaybiologia_com Contacto: [email protected]

5 months ago

¿Está la clave para evitar el Párkinson en tu intestino? https://t.co/oZV1Nzfnsb

Who to follow

CienciayBiología

@cienciaybio

Coca-Cola Ecuador

@CocaColaEC

#LaMagiaDeCreer está en cada reunión con tus amigos para ver los partidos de la Copa Mundial de la FIFA™

Carina Escobar Manero

@CarinaEscManero

Presidenta de la Plataforma de Organizaciones de Pacientes @pacientesPOP Consejo Nacional @aecc Secretaria General de @infoUNIMID

5 months ago

Un parásito común podría estar alterando tu personalidad ¿Y qué teiene que ver con los gatos? mira a continuación: https://t.co/xcRfoiQpIt

BiologiaC1's tweet photo. Un parásito común podría estar alterando tu personalidad

¿Y qué teiene que ver con los gatos? mira a continuación:
https://t.co/xcRfoiQpIt https://t.co/ZlYEeuEsKy

5 months ago

Tras dos décadas de experimentos, la ciencia confirma que los mamíferos no pueden clonarse indefinidamente sin colapsar genéticamente tras varias generaciones de clonación continua. Ciencias https://t.co/iOHfAOmSlp

BiologiaC1's tweet photo. Tras dos décadas de experimentos, la ciencia confirma que los mamíferos no pueden clonarse indefinidamente sin colapsar genéticamente tras varias generaciones de clonación continua. Ciencias

https://t.co/iOHfAOmSlp https://t.co/ouJe8kiaxS

5 months ago

Hallaron una especie de hongo parásito que invade y mata a las arañas de trampilla para luego emerger del cadáver para esparcir sus esporas. Ocurrió en la Mata Atlántica de Brasil. Flora y fauna https://t.co/pygK02Fwq4

BiologiaC1's tweet photo. Hallaron una especie de hongo parásito que invade y mata a las arañas de trampilla para luego emerger del cadáver para esparcir sus esporas. Ocurrió en la Mata Atlántica de Brasil. Flora y fauna

https://t.co/pygK02Fwq4 https://t.co/OqVeu1yQfa

5 months ago

Un tercio de la humanidad convive con el Toxoplasma gondii, un microorganismo que, lejos de ser un pasajero silencioso, parece capaz de manipular hilos invisibles en el cerebro humano, fomentando la aversión al riesgo. https://t.co/xcRfoiQpIt

BiologiaC1's tweet photo. Un tercio de la humanidad convive con el Toxoplasma gondii, un microorganismo que, lejos de ser un pasajero silencioso, parece capaz de manipular hilos invisibles en el cerebro humano, fomentando la aversión al riesgo.

https://t.co/xcRfoiQpIt https://t.co/3LSycyh8JC

5 months ago

Descubren con IA los genes que ayudan a las plantas a resistir estrés ambiental https://t.co/eO1oKv0zy4

BiologiaC1 retweeted

5 months ago

https://t.co/XmWlYOrluW

BiologiaC1 retweeted

5 months ago

https://t.co/urEPCymCGa

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BiologiaC1 retweeted

Niko McCarty.

@NikoMcCarty

6 months ago

A non-hyped explainer of the “cell simulation” paper. The recent study about the “4D” simulation of a minimal cell has been getting a lot of attention on social media. Unfortunately, most posts about it have serious errors. I’ve seen people claim that the model simulates every chemical reaction in the cell, for example, which is not true. Some biomolecules and reactions *are* tracked individually in the simulation, including proteins and RNA (and ribosomes), and the chromosome. But the simulation does not track individual metabolites (like ATP or glucose), water, nucleotide precursors, lipds, and so on. These "other" molecules are represented, instead, as concentrations (using ordinary differential equations). But anyway, here goes my quick explanation: Researchers built a computational model that simulates roughly 100 minutes of biological time, or one cell division, for a single bacterial cell. Each simulation takes 4–6 days to run on two NVIDIA A100 GPUs, and the authors ran it 50 times in replicate. The cell simulation includes some elements of randomness, so each replication attempt leads to a slightly different outcome. When they plotted out these replicates and averaged results, they found that the model could predict a few things without being fitted to experimental data: The simulated cells “divided” every 105 minutes, on average, which matches experimental results; and the mRNA molecules had an average half-life of 3.63 minutes, which is roughly what we’d expect from experiments, too. The cell they are modeling is called JCVI-syn3A, and it is not a naturally-occurring organism. It’s a bacterium that has been engineered, over many years, to have a small genome. It only has 493 genes (compared to 4,000+ for E. coli), all of which are housed on a single chromosome. The Syn3A cell was made by taking a natural organism, called Mycoplasma mycoides, and then slashing out non-essential genes. Its entire proteome, transcriptome, and metabolism have been studied in depth, which is why it’s being used to build these whole-cell simulations. The actual *simulation*, though, is not a single thing! Instead, the authors wrote down all the “stuff” that happens inside a cell (transcription! translation! metabolism! lipid biosynthesis!) and decided which type of mathematical model would be best-suited to describe each thing. Some cell processes were modelled deterministically, others had “spatial” elements, and other parts were relatively random. More specifically, they used four different types of models to build this simulation: 1. A Reaction-Diffusion Master Equation, which was used to model the individual proteins, RNAs, and ribosomes. 2. A Chemical Master Equation, which was used to model things where spatial location doesn’t matter as much (it basically treats the whole cell as one mixed entity); including tRNA charging. 3. Ordinary Differential Equations, which you may be familiar with from Calculus class, were used to model changes in ATP concentration, lipids, and so on. 4. Brownian Dynamics, which simulated the chromosome as a physical chain of beads, where each bead represents 10 base pairs of DNA. The Reaction-Diffusion Equation works like this: Basically, they chopped up the entire digital cell into a 3D grid of cubes. Each cube measures 10 nanometers on each side. The whole cell is about 500 nanometers across, so there are tens of thousands of cubes in the cell's interior. (This is a useful way to coarse grain the simulation; if the cubes were smaller, the simulation would take much longer to run.) Each cube is a little box that contains some number of molecules. At every “step” in the simulation, only one of two things can happen to the molecules in each box: Either they react with a molecule in the same box, or they diffuse (“hop”) to an adjacent box. That’s it; the model is just rolling a die for each molecule at each time step in each box, and using those results to decide how each molecule changes over time. (The reason this spatial model is important is because biology only works if molecules physically bump into each other. And so this spatial grid means that, unlike simpler models, a protein actually has to “diffuse” across boxes in the cell to encounter its reaction partner; only then can it react and do something useful.) So anyway, each of these models is used to represent a different type of molecule. It’s not like there is a single, all-powerful simulation that they are running here; instead, they’re running these four models together, using a script that synchronizes their results with each other. The Reaction-Diffusion equation is the main part of the simulation. It takes time steps of 50 microseconds of biological time. Every 12.5 milliseconds of biological time — meaning every 250 RDME steps — the simulation pauses so that the other models can synchronize based on the latest state of the simulation. The Brownian Dynamics part runs on a completely separate GPU, and only updates every four seconds of biological time. So that's the gist here. But let's also be honest about what this simulation does NOT do: - It does not include polysomes, which are a cluster of ribosomes that all latch onto a single mRNA and translate at the same time. Polysomes are really common inside of cells, but this simulation assumes that each mRNA can only be translated by one ribosome at a time. - It does not include polycistronic transcription. In bacteria, genes are often grouped next to each other on the chromosome and thus “transcribed” (or turned into mRNA) all at once, together. The majority of genes in E. coli, for example, are arranged in these operons, and the authors of this paper acknowledge that many Syn3A genes are likely co-transcribed the same way. But the simulation doesn't capture it. - The authors manually tuned many parameters to get the model to make predictions that more closely resemble experiments. Earlier simulations were waaaayyyyy off from experimental results. For example, they adjusted the ratio of mRNA binding rates to ribosomes versus degradosomes because, in earlier simulations, mRNA was being degraded too quickly, before ribosomes could translate it, causing most proteins to be severely underproduced. - In the Brownian Dynamics model, the authors added a “fake” 12 pN physical force to push the two daughter chromosomes apart during division, because the real biological mechanism for chromosome partitioning in Syn3A is not known. - And some other things. That being said: This model is really cool! I love papers like this! I'm enamored by scientists who choose really difficult problems (like simulating an entire cell) and actually go after it and make progress! This paper is amazing because it shows us what we are able to simulate well, and what we don't yet understand, and to figure out which experiments we ought to perform to reconcile the two. So instead of framing this paper as "OH MY GOSH SCIENTISTS FIGURED OUT HOW TO SIMULATE AN ENTIRE CELL!" we should frame it as proof that there is still plenty of room at the bottom, many measurements to be made, and many avenues to explore as we seek to understand biology better.

NikoMcCarty's tweet photo. A non-hyped explainer of the “cell simulation” paper.

The recent study about the “4D” simulation of a minimal cell has been getting a lot of attention on social media. Unfortunately, most posts about it have serious errors. I’ve seen people claim that the model simulates every chemical reaction in the cell, for example, which is not true.

Some biomolecules and reactions *are* tracked individually in the simulation, including proteins and RNA (and ribosomes), and the chromosome. But the simulation does not track individual metabolites (like ATP or glucose), water, nucleotide precursors, lipds, and so on. These "other" molecules are represented, instead, as concentrations (using ordinary differential equations).

But anyway, here goes my quick explanation:

Researchers built a computational model that simulates roughly 100 minutes of biological time, or one cell division, for a single bacterial cell. Each simulation takes 4–6 days to run on two NVIDIA A100 GPUs, and the authors ran it 50 times in replicate. The cell simulation includes some elements of randomness, so each replication attempt leads to a slightly different outcome. When they plotted out these replicates and averaged results, they found that the model could predict a few things without being fitted to experimental data: The simulated cells “divided” every 105 minutes, on average, which matches experimental results; and the mRNA molecules had an average half-life of 3.63 minutes, which is roughly what we’d expect from experiments, too.

The cell they are modeling is called JCVI-syn3A, and it is not a naturally-occurring organism. It’s a bacterium that has been engineered, over many years, to have a small genome. It only has 493 genes (compared to 4,000+ for E. coli), all of which are housed on a single chromosome. The Syn3A cell was made by taking a natural organism, called Mycoplasma mycoides, and then slashing out non-essential genes. Its entire proteome, transcriptome, and metabolism have been studied in depth, which is why it’s being used to build these whole-cell simulations.

The actual *simulation*, though, is not a single thing! Instead, the authors wrote down all the “stuff” that happens inside a cell (transcription! translation! metabolism! lipid biosynthesis!) and decided which type of mathematical model would be best-suited to describe each thing. Some cell processes were modelled deterministically, others had “spatial” elements, and other parts were relatively random.

More specifically, they used four different types of models to build this simulation:

1. A Reaction-Diffusion Master Equation, which was used to model the individual proteins, RNAs, and ribosomes.
2. A Chemical Master Equation, which was used to model things where spatial location doesn’t matter as much (it basically treats the whole cell as one mixed entity); including tRNA charging.
3. Ordinary Differential Equations, which you may be familiar with from Calculus class, were used to model changes in ATP concentration, lipids, and so on.
4. Brownian Dynamics, which simulated the chromosome as a physical chain of beads, where each bead represents 10 base pairs of DNA.

The Reaction-Diffusion Equation works like this: Basically, they chopped up the entire digital cell into a 3D grid of cubes. Each cube measures 10 nanometers on each side. The whole cell is about 500 nanometers across, so there are tens of thousands of cubes in the cell's interior. (This is a useful way to coarse grain the simulation; if the cubes were smaller, the simulation would take much longer to run.)

Each cube is a little box that contains some number of molecules. At every “step” in the simulation, only one of two things can happen to the molecules in each box: Either they react with a molecule in the same box, or they diffuse (“hop”) to an adjacent box. That’s it; the model is just rolling a die for each molecule at each time step in each box, and using those results to decide how each molecule changes over time.

(The reason this spatial model is important is because biology only works if molecules physically bump into each other. And so this spatial grid means that, unlike simpler models, a protein actually has to “diffuse” across boxes in the cell to encounter its reaction partner; only then can it react and do something useful.)

So anyway, each of these models is used to represent a different type of molecule. It’s not like there is a single, all-powerful simulation that they are running here; instead, they’re running these four models together, using a script that synchronizes their results with each other.

The Reaction-Diffusion equation is the main part of the simulation. It takes time steps of 50 microseconds of biological time. Every 12.5 milliseconds of biological time — meaning every 250 RDME steps — the simulation pauses so that the other models can synchronize based on the latest state of the simulation. The Brownian Dynamics part runs on a completely separate GPU, and only updates every four seconds of biological time.

So that's the gist here. But let's also be honest about what this simulation does NOT do:

- It does not include polysomes, which are a cluster of ribosomes that all latch onto a single mRNA and translate at the same time. Polysomes are really common inside of cells, but this simulation assumes that each mRNA can only be translated by one ribosome at a time.
- It does not include polycistronic transcription. In bacteria, genes are often grouped next to each other on the chromosome and thus “transcribed” (or turned into mRNA) all at once, together. The majority of genes in E. coli, for example, are arranged in these operons, and the authors of this paper acknowledge that many Syn3A genes are likely co-transcribed the same way. But the simulation doesn't capture it.
- The authors manually tuned many parameters to get the model to make predictions that more closely resemble experiments. Earlier simulations were waaaayyyyy off from experimental results. For example, they adjusted the ratio of mRNA binding rates to ribosomes versus degradosomes because, in earlier simulations, mRNA was being degraded too quickly, before ribosomes could translate it, causing most proteins to be severely underproduced.
- In the Brownian Dynamics model, the authors added a “fake” 12 pN physical force to push the two daughter chromosomes apart during division, because the real biological mechanism for chromosome partitioning in Syn3A is not known.
- And some other things.

That being said: This model is really cool! I love papers like this! I'm enamored by scientists who choose really difficult problems (like simulating an entire cell) and actually go after it and make progress!

This paper is amazing because it shows us what we are able to simulate well, and what we don't yet understand, and to figure out which experiments we ought to perform to reconcile the two. So instead of framing this paper as "OH MY GOSH SCIENTISTS FIGURED OUT HOW TO SIMULATE AN ENTIRE CELL!" we should frame it as proof that there is still plenty of room at the bottom, many measurements to be made, and many avenues to explore as we seek to understand biology better.

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BiologiaC1 retweeted

6 months ago

https://t.co/7q8B0rTX7Q

BiologiaC1 retweeted

Micah G. Allen

@micahgallen

6 months ago

A recent study in Nature Communications reveals over 250 metabolic enzymes located directly on chromatin, a discovery that vastly expands the previously known count of only about 20. https://t.co/8ucPDDVX01

micahgallen's tweet photo. A recent study in Nature Communications reveals over 250 metabolic enzymes located directly on chromatin, a discovery that vastly expands the previously known count of only about 20.
https://t.co/8ucPDDVX01 https://t.co/QGtnYdBZzT

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Jose Ramos Vivas

@joseramosvivas

6 months ago

🙀Brutal.. ¿Sabías que podemos "reprogramar" astrocitos (un tipo de células del cerebro) para que limpien la basura que causa el Alzheimer? - Un artículo salido del horno en Science revela cómo los astrocitos modificados genéticamente (CAR-As) pueden ser nuestros mejores aliados. 👇🧫 - El problema son las placas de proteína beta-amiloide que destruyen las neuronas.🚀 Pero los Científicos han diseñado astrocitos con receptores quiméricos (CAR) que detectan y "se comen" (fagocitan) estas placas de forma específica. 💉 Método: usan un virus inofensivo (AAV) inyectado en sangre que llega al cerebro y solo activa a los astrocitos. ✅ Resultado: menos placas, neuronas más sanas y una respuesta inflamatoria mucho más equilibrada que con los tratamientos actuales. Me parece impresionante... 🧬🔬#Alzheimer #Neurociencia #Biotecnología #SaludMental #Ciencia #Innovación #Genética #Investigación #Science 👇 https://t.co/HcqpXjbNVI

joseramosvivas's tweet photo. 🙀Brutal.. ¿Sabías que podemos "reprogramar" astrocitos (un tipo de células del cerebro) para que limpien la basura que causa el Alzheimer?
- Un artículo salido del horno en Science revela cómo los astrocitos modificados genéticamente (CAR-As) pueden ser nuestros mejores aliados. 👇🧫
- El problema son las placas de proteína beta-amiloide que destruyen las neuronas.🚀
Pero los Científicos han diseñado astrocitos con receptores quiméricos (CAR) que detectan y "se comen" (fagocitan) estas placas de forma específica.
💉 Método: usan un virus inofensivo (AAV) inyectado en sangre que llega al cerebro y solo activa a los astrocitos.
✅ Resultado: menos placas, neuronas más sanas y una respuesta inflamatoria mucho más equilibrada que con los tratamientos actuales.

Me parece impresionante... 🧬🔬#Alzheimer #Neurociencia #Biotecnología #SaludMental #Ciencia #Innovación #Genética #Investigación #Science
👇
https://t.co/HcqpXjbNVI

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BiologiaC1 retweeted

6 months ago

https://t.co/jCtmfoJCGB

BiologiaC1 retweeted

6 months ago

https://t.co/R9qPyjf8Tt

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6 months ago

El laboratorio australiano Cortical Labs ha logrado un avance fascinante en computación biológica: un sistema llamado CL1 que utiliza alrededor de 200.000 neuronas humanas cultivadas en laboratorio ha aprendido a jugar Doom, el clásico videojuego de shooting de 1993. Click aquí para más información: https://t.co/5QN6yV6JZ6

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6 months ago

https://t.co/knAmbmmJdu

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