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Transcriptional readthrough at Atf4 locus suppresses Rps19bp1 and impairs heart development.

Zengming Zhang1, Tongbin Wu2, Zeyu Chen1

  • 1Department of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.

Cardiovascular Research
|November 17, 2025
PubMed
Summary

Cardiac development relies on RPS19BP1, not ATF4. Deleting the Atf4 polyA signal caused readthrough, downregulating RPS19BP1 and leading to cardiac defects. This highlights potential artifacts in previous Atf4 knockout models.

Keywords:
ATF4Rps19bp1Transcriptional Readthroughheart developmentknockout

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Area of Science:

  • Cardiovascular Biology
  • Molecular Genetics
  • Transcriptional Regulation

Background:

  • Activating Transcription Factor 4 (ATF4) is a key regulator in various physiological and pathological conditions.
  • Previous research linked ATF4 to cardiomyocyte death in heart diseases, but its role in developing cardiomyocytes was unknown.

Purpose of the Study:

  • To investigate the role of ATF4 in cardiomyocyte development.
  • To generate and analyze novel mouse models for studying ATF4 function in the heart.

Main Methods:

  • Generated cardiomyocyte-specific and global Atf4 knockout mouse models.
  • Created cardiomyocyte-specific Rps19bp1 deletion models.
  • Performed detailed morphological and molecular analyses of cardiac phenotypes.

Main Results:

  • Cardiomyocyte-specific Atf4 knockout with polyA deletion (Atf4cKO(e2/3/pA)) caused severe cardiac defects and embryonic lethality.
  • These defects were attributed to Rps19bp1 downregulation due to transcriptional readthrough from the deleted Atf4 polyA signal.
  • Atf4 knockout models without polyA signal deletion (Atf47del/7del, Atf41ins/1ins) showed normal cardiac development.
  • Cardiomyocyte-specific Rps19bp1 deletion recapitulated the cardiac defects observed in Atf4cKO(e2/3/pA) mice.

Conclusions:

  • Cardiac phenotypes in Atf4cKO(e2/3/pA) mice result from Rps19bp1 downregulation, not loss of ATF4 function.
  • Transcriptional readthrough and Rps19bp1 downregulation are likely confounding factors in previously reported Atf4 knockout studies.
  • RPS19BP1 plays an essential role in cardiac development, and locus-dependent transcriptional interference mechanisms must be considered in genetic model studies.