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Updated: Feb 5, 2026

Tuning Degradation to Achieve Specific and Efficient Protein Depletion
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RCC1 depletion drives protein transport defects and rupture in micronuclei

Molly G Zych1,2, Maya Contreras2, Anna E Mammel2

  • 1Molecular and Cellular Biology PhD Program, University of Washington , Seattle, WA, USA.

The Journal of Cell Biology
|February 3, 2026
PubMed

Insights

Micronuclei (MN) rupture due to impaired protein export and excessive growth, causing nuclear lamina defects. Increasing the transport protein RCC1 can prevent MN rupture and instability, impacting cancer development.

Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • Micronuclei (MN) are indicators of chromosome instability and their rupture has protumorigenic effects.
  • Nuclear lamina defects are known to precede MN rupture, but the causes are not fully understood.

Purpose of the Study:

  • To elucidate the underlying mechanisms causing nuclear lamina defects and subsequent rupture in micronuclei.
  • To investigate the role of the transport protein RCC1 in micronuclear stability and rupture.

Main Methods:

  • Analyzing the relationship between micronuclear growth, protein export, and nuclear lamina integrity.
  • Manipulating RCC1 levels (overexpression and loss) in micronuclei to assess its impact on protein transport and rupture.
  • Investigating the influence of chromatin state (euchromatin) on RCC1 levels and micronuclear stability.

Main Results:

  • Micronuclear lamina gaps are caused by excessive MN growth due to impaired protein export, linked to reduced RCC1 levels.
  • Overexpression of RCC1 enhances protein export and protects MN from rupture.
  • Chromatin state influences MN stability; euchromatic MN with RCC1 loss experience impaired protein import, accelerating rupture when RCC1 is increased.

Conclusions:

  • A novel model for MN rupture is proposed, involving impaired protein export, continuous MN growth, and nuclear lamina defects.
  • Chromatin-specific features modulate the rupture of small MN by affecting nuclear transport.
  • Targeting RCC1 levels presents a potential strategy to control MN stability and its protumorigenic consequences.

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