Making Cells and Proteins Resources

Lesson 1: From Gene to Protein – Building CFTR

Remember CFTR from our last module? That finicky protein channel that causes cystic fibrosis when it doesn’t work? Well, here’s the million-dollar question: how does your body actually MAKE CFTR in the first place? We’re about to trace the journey from a recipe written in DNA all the way to a functional protein sitting in your cell membrane. Spoiler alert: it involves copying, translating, and a whole lot of molecular machinery that would make a factory jealous.

Think about it this way: your cells have been making CFTR proteins since before you were born. Every single respiratory epithelial cell in your airways contains the CFTR gene on chromosome 7, and that gene gets read thousands of times to produce the proteins you need. The process is called protein synthesis, and it’s happening in your body right now as you read this. Today we’re going to follow the step-by-step instructions that turn a sequence of nucleotides (DNA) into a sequence of amino acids (protein), and you’ll see exactly where things go wrong in cystic fibrosis.

Key Concepts:

  • DNA Structure as Information Storage – The CFTR gene is a specific sequence of nucleotides on chromosome 7 that contains the instructions for building the CFTR protein
  • Transcription: DNA → RNA – Making a disposable mRNA copy of the CFTR gene that can travel from the nucleus to the ribosomes
  • Translation: RNA → Protein – Ribosomes read the mRNA sequence and assemble amino acids in the correct order to build the CFTR pro
Chart illustrating the genetic code, displaying codons and their corresponding amino acids.

Pre Class Lectures

  • DNA Structure 12 minutes
  • DNA to RNA (Transcription) 13 minutes
  • RNA to Protein (Translation) 17 minutes

Post Class Lectures

  • The Cell Cycle 15 minutes

Lesson 2: DNA Replication – Copying the CFTR Recipe

Your body makes about 25 million new cells every second. That’s 25 million times per second that your DNA needs to be copied PERFECTLY, including the CFTR gene on chromosome 7. One copying mistake in the CFTR gene, and boom—you might have a daughter cell that can’t make functional CFTR protein. So how does your body pull off this miracle of precision copying? And more importantly, what happens when it doesn’t?

Here’s the thing about DNA replication: it has to be both incredibly fast and incredibly accurate. Your cells use an enzyme called DNA polymerase that reads the original DNA strand and builds a complementary new strand using base pairing rules. When everything works correctly, you get two identical copies of chromosome 7, each with a perfect CFTR gene. But sometimes—rarely, but sometimes—DNA polymerase makes a mistake. It might insert the wrong nucleotide, or skip one entirely, or add an extra one. These mistakes are called mutations, and they’re exactly how CF started in the first place. Someone’s ancestor, generations ago, had a DNA replication error in the CFTR gene, and that mutation has been faithfully copied and passed down through families ever since. Today we’re going to understand how DNA replication usually prevents these disasters, and what happens on the rare occasions when it fails.

Key Concepts:

  • DNA Replication Ensures Genetic Continuity – Before any cell divides, it must duplicate all 46 chromosomes so each daughter cell gets a complete set of genetic instructions, including the CFTR gene
  • Semi-Conservative Replication – Each new DNA molecule contains one original strand and one newly synthesized strand, ensuring accurate copying through base pairing
  • Replication Errors Create Mutations – When DNA polymerase makes mistakes copying the CFTR gene, the result is a mutation that may cause cystic fibrosis if passed to offspring
Illustration depicting the process of gene expression, showing the transition from DNA to mRNA to protein.
The flow of information for making a protein from the recipe encoded in the DNA.

Pre Class Lectures

Post Class Lectures

Lesson 3: The Cell Cycle & Mitosis – Distributing CFTR Genes

Let’s talk about the most elegant choreography in biology: mitosis. Your cells are constantly dividing to replace damaged ones (remember when you burned your mouth on hot pizza?), and every single time they divide, they have to perfectly distribute 46 chromosomes—including chromosome 7 with your CFTR gene—into two daughter cells. It’s like a molecular custody battle, except both kids get EVERYTHING. And when it goes wrong? Well, that’s how you get cells with too many chromosomes, too few chromosomes, or that wonderful thing we call cancer. No pressure, cellular machinery!

The respiratory epithelial cells lining your airways are some of the hardest-working cells in your body when it comes to division. They’re constantly exposed to dust, pollution, and irritants, so they need to be replaced regularly through mitosis. Every time one of these cells divides, it goes through a carefully orchestrated series of steps: the chromosomes condense, line up in the middle of the cell, get pulled apart to opposite ends, and finally separate into two new cells. Each daughter cell receives exactly 23 pairs of chromosomes, including one copy of chromosome 7 with the CFTR gene. Those daughter cells will then use their CFTR genes to make CFTR proteins, continuing the cycle. But here’s what makes mitosis so critical for CF patients: if you have a mutated CFTR gene, every single new cell produced through mitosis will also have that mutated gene. That’s why CF affects so many tissues—the mutation gets copied and distributed to every cell in the body.

Key Concepts:

  • The Cell Cycle Prepares Cells for Division – During interphase (G1, S, G2 phases), cells grow, replicate their DNA including the CFTR gene, and prepare all cellular components for division
  • Mitosis Distributes Chromosomes Equally – The phases of mitosis (prophase, metaphase, anaphase, telophase) ensure each daughter cell receives exactly one copy of each chromosome, including chromosome 7 with the CFTR gene
  • Checkpoints Prevent Disasters – The cell has quality control mechanisms that detect errors in chromosome alignment or DNA damage and trigger cell death (apoptosis) if problems can’t be fixed
Chromosomal karyotype representation showing pairs of chromosomes in different colors, illustrating genetic information.
A Karyotype showing the homologous chromosomes for each of the 23 pairs.

Pre Class Lectures

Post Class Lectures

Lesson 4: Putting It All Together – The CFTR Life Cycle

We’ve journeyed from DNA structure to protein synthesis to cell division. Now it’s time for the big reveal: how does a single fertilized egg with one copy of the CFTR gene from each parent turn into YOU, with trillions of cells all making CFTR protein? We’re going to trace the complete life cycle: from your parents passing down CFTR genes, to those genes being replicated billions of times, to those genes being transcribed and translated in every respiratory epithelial cell you make. This is the grand finale where molecular biology becomes human biology.

Here’s the complete story: You inherited two copies of chromosome 7—one from your biological mother and one from your biological father. Each chromosome 7 carries a CFTR gene. If you don’t have CF, both of those genes contain the correct sequence to make functional CFTR protein. From the moment you were conceived as a single fertilized egg, your cells have been going through this cycle over and over: (1) DNA replication copies your CFTR genes, (2) mitosis distributes those copies to daughter cells, (3) those daughter cells use transcription and translation to make CFTR proteins, (4) the cells eventually divide again, and the cycle repeats. This process has happened trillions of times to build your body. But if someone has CF, they inherited two mutated CFTR genes, and that mutation gets faithfully copied and distributed to every cell through DNA replication and mitosis. That’s why gene therapy is so challenging—you can’t just fix one cell’s CFTR gene; you’d need to fix it in billions of cells across multiple tissues. Today we’re going to see how all these processes work together as an integrated system that maintains genetic information across your entire lifetime.

Key Concepts:

  • Inheritance → Replication → Division → Protein Synthesis Forms an Integrated Cycle – The CFTR genes you inherited get replicated before every cell division, distributed to daughter cells through mitosis, and then used to make proteins through transcription and translation
  • CF is a Genetic Disease Because Mutations Are Copied and Distributed – A mutated CFTR gene gets replicated with the same fidelity as a normal gene, meaning every cell descended from the fertilized egg will carry that same mutation
  • Understanding the Cycle Explains Why Treatment is Complex – Since the mutated CFTR gene exists in trillions of cells throughout the body, any genetic treatment would need to reach and correct the gene in vast numbers of cells across multiple tissue types
Illustration of the trachea and lungs shows a cross-section of the trachea wall, which is made up of pseudostratified ciliated columnar epithelium. Cilia extend into the lumen. A zoomed-in portion of the wall shows how CFTR protein transports chloride ions, while another transporter moves sodium, to bring water into the mucus layer.
Trachea anatomy showing pseudostratified ciliated epithelium including CFTR protein function at the lung epithelial cell.

Pre Class Lectures

Post Class Lectures

List of terms