Gene Expression
Thus, the mechanism of action of steroid hormones is to modulate gene expression in target cells.
Gene Expression
- B-DNA plays a key role in gene expression . Its hydrated and less compact structure allows enzymes to access the genetic code and catalyze transcription, making it essential for the central dogma of molecular biology.
Read this in Tertiary Structure of DNA
Gene Expression
- Due to its tightly packed structure and reduced hydration, A-DNA is not involved in gene expression . Its compactness limits interactions with enzymes and proteins required for transcription.
Read this in Tertiary Structure of DNA
Gene Expression
- Z-DNA is generally not involved in gene expression. Its tightly packed structure and lack of hydration prevent interaction with the enzymes required for transcription.
Read this in Tertiary Structure of DNA
What our notes say
- Thus, the mechanism of action of steroid hormones is to modulate gene expression in target cells. (Medical Physiology Assorted SAQs — With Answers (Past Paper Study Guide))
- *MYC is a master transcriptional driver of glycolytic gene expression, directly supporting the Warburg phenotype.* (General Pathology MCQs: Cancer, Tumors & Molecular Path Review)
- Contains viral proteins that are immediately active upon cell entry — before viral gene expression begins (EXAM: Basic Virology, Viral Replication, Prions & Slow Viruses, Poxviruses & VZV)
- Epigenetic changes — Heritable modifications in gene expression (e.g., via DNA methylation or histone modification) that occur without altering the underlying DNA sequence. (Cytopathology vs Histopathology CAT: Definitions & Lab Basics)
- Others: distant metastases, tumor size, locally advanced disease (skin/muscle invasion), lymphovascular invasion, inflammatory carcinoma (dermal lymphatic invasion, 3-yr survival only 3–10%), gene expression profiling, response to neoadjuvant chemo (Exam Prep: Skin Infections, Psoriasis & Pemphigus)
- Epigenetics — heritable changes in gene expression without altering DNA sequence (Genetic Disorders Pathology Crash Course: Exam Revision Notes)
Study material on Gene Expression
- Tertiary Structure of DNA
- Transcription Factors
- Medical Biochemistry, Genetics, and Molecular Biology
- Introduction To Genetics
- LECTURE 1: Principles of Endocrinology
- Mbchb Cat - Genetics Answer Key
- EXAM: Bacteriophages, Laboratory Diagnosis, HPV & Parvovirus B19
- EXAM: Basic Virology, Viral Replication, Prions & Slow Viruses, Poxviruses & VZV
- Mbchb Cat - Genetics Answer Key MCQs
- Molecular Biology,Molecular Genetics & Microbial-Biochemistry LAQs & SAQs
Practice questions on Gene Expression
In cardiac hypertrophy, the switch from adult to fetal gene expression includes:
- Replacement of β-myosin heavy chain with α isoform
- Replacement of α-myosin heavy chain with β isoform
- Increased expression of telomerase
- Downregulation of atrial natriuretic factor
Answer: B. Hypertrophic hearts switch from α-myosin (fast, high energy consumption) to β-myosin (slow, more energetically economical) heavy chain—a fetal isoform. ANF is INCREASED (not decreased), acting as a compensatory hormone to reduce blood volume and pressure. This gene switching represents an attempt to reduce energy consumption but may impair contractility. ---
Gene expression in Mendelian disorders may be
- Only dominant
- Only recessive
- Dominant, recessive, or co-dominant
- Always co-dominant
- Occurs only after chronic exposure
Answer: A. Gene expression in Mendelian disorders can be dominant (one mutant allele sufficient), recessive (two mutant alleles needed), or co-dominant (both alleles expressed). ---
Recent gene expression profiling of breast cancers challenges traditional metastasis theory by suggesting
- Metastasis always requires late-stage mutations
- Some tumors acquire metastatic capability early during carcinogenesis
- All tumors contain metastatic subclones from the beginning
- Metastasis is independent of the primary tumor genotype
Answer: B. ** Gene profiling shows some breast cancers have a metastasis-like signature early on, before clinical metastasis is apparent. This suggests that metastatic capability can be an intrinsic property developed during early carcinogenesis, not just from late-stage random mutations creating metastatic subclones. ---