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Autophagy is essential for human myelopoiesis

Jiaming Gu1, Yanling Zhu2, Huaisong Lin2

  • 1CAS Key Laboratory of Regenerative Biology, Guangzhou Institutes of Biomedicine and Health, Centre for Regenerative Medicine and Health, Hong Kong Institute of Science and Innovation, Hong Kong, Chinese Academy of Sciences, Guangzhou 510530, China; University of Chinese Academy of Sciences, Beijing 100049, China; Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, Center for Cell Lineage and Development, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China.

Stem Cell Reports
|January 12, 2024
PubMed

Insights

Autophagy factor ATG7 is crucial for rapid proliferation of myeloid progenitors during emergency myelopoiesis. ATG7 deficiency impairs this process by affecting p53 regulation, highlighting a new role for autophagy in immune defense.

Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Biology

Background:

  • Emergency myelopoiesis (EM) rapidly replenishes myeloid cells for immune defense.
  • A critical step in EM is the transition of quiescent hematopoietic stem cells (HSCs) to highly proliferative myeloid progenitors (MPs).
  • Regulation of MP proliferation during EM is not well understood.

Purpose of the Study:

  • To investigate the role of autophagy factor ATG7 in regulating myeloid progenitor proliferation during human emergency myelopoiesis.
  • To elucidate the molecular mechanisms by which ATG7 influences MP proliferation.

Main Methods:

  • Utilized peripheral blood (PB)-mobilized hematopoietic stem/progenitor cells (HSPCs) with ATG7 knockdown.
  • Generated HSPCs from ATG7 knockout human embryonic stem cells (hESCs).
  • Analyzed cell proliferation and p53 localization in lysosomes.

Main Results:

  • ATG7 deficiency in HSPCs severely impaired proliferation during the transition to MPs.
  • ATG7-deficient cells showed defects in the cell-cycle switch required for rapid proliferation.
  • ATG7 deficiency led to reduced lysosomal localization of p53, suggesting impaired autophagy-mediated degradation.

Conclusions:

  • ATG7 is essential for the rapid proliferation of myeloid progenitors during human emergency myelopoiesis.
  • Autophagy, mediated by ATG7, plays a previously unrecognized role in regulating p53 for efficient MP proliferation.
  • This finding sheds light on the molecular control of immune cell replenishment.

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