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<p>The&#xa0;<i>Drosophila</i>&#xa0;midgut epithelium undergoes nutrient-dependent growth regulated by the InR-Akt-TOR signaling pathway, though the downstream transducers that coordinate this response remain incompletely defined. We demonstrate that&#xa0;<i>hipk</i>&#xa0;is selectively expressed in intestinal stem cells (ISCs) and their immediate progeny, enteroblasts (EBs), the transient precursors to the absorptive enterocytes (ECs) that form the bulk of the gut epithelium.&#xa0;<i>Hipk</i>&#xa0;expression is dynamically regulated by nutritional status and requires active InR-Akt-TOR signaling; notably, ectopic activation of this pathway is sufficient to induce&#xa0;<i>hipk</i>&#xa0;expression even under nutrient-restricted conditions. Through genetic analysis, we show that Hipk promotes ISC proliferation while simultaneously directing lineage specification toward the EB fate, thereby facilitating expansion of the absorptive epithelium in response to nutrient availability. These findings establish Hipk as a critical nutrient-responsive effector that couples insulin signaling to both stem cell division and lineage commitment in the adult intestine.</p>

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Hipk transduces nutrient signals to control intestinal stem cell proliferation and fate in Drosophila

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月24日

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  • Xiaojie Wu,
  • Hyunju Kim,
  • Wijeong Jang,
  • Changsoo Kim

摘要

The Drosophila midgut epithelium undergoes nutrient-dependent growth regulated by the InR-Akt-TOR signaling pathway, though the downstream transducers that coordinate this response remain incompletely defined. We demonstrate that hipk is selectively expressed in intestinal stem cells (ISCs) and their immediate progeny, enteroblasts (EBs), the transient precursors to the absorptive enterocytes (ECs) that form the bulk of the gut epithelium. Hipk expression is dynamically regulated by nutritional status and requires active InR-Akt-TOR signaling; notably, ectopic activation of this pathway is sufficient to induce hipk expression even under nutrient-restricted conditions. Through genetic analysis, we show that Hipk promotes ISC proliferation while simultaneously directing lineage specification toward the EB fate, thereby facilitating expansion of the absorptive epithelium in response to nutrient availability. These findings establish Hipk as a critical nutrient-responsive effector that couples insulin signaling to both stem cell division and lineage commitment in the adult intestine.