BRCA1 tumor suppressor biology: Which mechanism best explains how inherited BRCA1 helps regulate cell division and maintain genome integrity?

Introduction / Context:
BRCA1 is a classic tumor suppressor whose germline mutations increase the risk of breast and ovarian cancers. The question asks you to identify the molecular mechanism by which BRCA1 regulates cell division through genome maintenance.

Given Data / Assumptions:

• BRCA1 participates in DNA damage response pathways.
• Homologous recombination (HR) requires RAD51-mediated strand invasion.
• Tumor suppressors typically prevent unchecked division by ensuring accurate DNA repair or triggering checkpoints.

Concept / Approach:
BRCA1 functions in double-strand break repair, checkpoint control, and chromatin remodeling. A key function is promoting homologous recombination through interactions with RAD51, coordinating repair to preserve genomic stability. Loss of BRCA1 impairs HR, increases genomic instability, and thus predisposes to tumorigenesis.

Step-by-Step Solution:
Identify the pathway: DNA double-strand break repair via homologous recombination.Recall BRCA1–RAD51 functional linkage in assembling repair foci.Conclude: BRCA1 helps regulate division by binding RAD51 to facilitate accurate repair.

Verification / Alternative check:
Cells lacking BRCA1 show defective RAD51 focus formation and hypersensitivity to DNA-damaging agents; PARP inhibitor sensitivity further supports HR deficiency.

Why Other Options Are Wrong:

• Promoter activation of mitosis is not a canonical BRCA1 role.
• Cyclin complexing is characteristic of CDKs and cyclins, not BRCA1.
• Outer membrane binding and receptor blockade are not BRCA1 mechanisms.

Common Pitfalls:
Confusing BRCA1 with generalized cell cycle drivers (cyclins/CDKs) or membrane receptors. BRCA1 is primarily a guardian of genome integrity.

Final Answer:
binding to the recombination protein RAD51 to facilitate DNA damage repair