# Endosomal Microautophagy in Drosophila

> **NIH NIH R01** · ALBERT EINSTEIN COLLEGE OF MEDICINE · 2020 · $464,230

## Abstract

Endosomal Microautophagy in Drosophila
 Proper turnover of proteins and organelles is essential for normal cell function.
Damaged or altered cytosolic proteins are cleared by the proteasome and autophagy.
Importantly, autophagy has the additional role of providing nutrients to cells under stress
conditions such as starvation, and is thus essential for energy balance. The liver is one
of the main regulators of lipids in the body and has major roles in metabolism such as
gluconeogenesis, a process that is particularly dependent on amino acids generated by
autophagic degradation of cellular proteins under starvation or stress. Furthermore,
removal of damaged organelles and aggregated proteins is essential to protect liver and
kidneys against age related disorders.
Macroautophagy (MA), Chaperone mediated Autophagy (CMA) and endosomal
Microautophagy (eMI) are the three major forms of autophagy. MA engulfs bulk-regions
of cytoplasm including organelles in a double membrane vesicle (autophagosome).
Autophagosome fusion with lysosomes leads to the degradation of the engulfed material.
Less is known about CMA and eMI, which mostly degrade proteins containing a
targeting motif (KFERQ related sequences) that is recognized by the cytoplasmic Hsc70.
During eMI, which to date has only been characterized biochemically and by EM,
KFERQ containing substrates bound to Hsc70 are taken up into multivesicular
bodies/late endosomes in an ESCRT machinery dependent process and degraded.
Previously, the existence of eMI beyond mammals was unknown and there is currently
no in vivo system to study mammalian eMI. Hence, the genetic power of model
organisms such as Drosophila have not been exploited for the study of KFERQ-
dependent forms of autophagy.
Using a fluorescently tagged model substrate expressed in transgenic flies, we
developed a model system to study starvation inducible eMI in vivo. Using this system,
we will assess the physiological function and regulation of eMI by starvation and other
forms of cellular stress. Furthermore, we will characterize regulators of eMI that we
have identified in a genetic screen.

## Key facts

- **NIH application ID:** 9884777
- **Project number:** 5R01GM119160-05
- **Recipient organization:** ALBERT EINSTEIN COLLEGE OF MEDICINE
- **Principal Investigator:** ANDREAS JENNY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $464,230
- **Award type:** 5
- **Project period:** 2017-02-01 → 2021-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9884777

## Citation

> US National Institutes of Health, RePORTER application 9884777, Endosomal Microautophagy in Drosophila (5R01GM119160-05). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/9884777. Licensed CC0.

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