Event Title

Autophagy Gene Ulk1B Potentially Responsible For Yolk Digestion In Zebrafish (Danio Rerio) Embryos

Location

SU 214

Start Date

19-4-2019 9:00 AM

Department

Biology

Session

Session 5

Description

Autophagy or “self-eating” is essential for a cell to maintain energy balance and overturn damaged organelles. The Ulk1b complex is a serine/threonine protein kinase responsible for autophagosome maturation and autophagy initiation. ulk1b is activated by starvation in response to glucose deficiency signals. Here, we are investigating if yolk digestion is a form autophagy carried out by the ulk1b complex. Our aim is to understand autophagy in the yolk and establish the zebrafish yolk cell as a novel system to study digestion. Within the yolk, yolk granules are present to provide nutrients needed for embryonic development. Thus, we hypothesize that if yolk digestion is a form of autophagy, knockdown of ulk1b will halt yolk digestion. To knockdown ulk1b, we will use CRISPRi, or CRISPR-mediated inhibition and study the effect on zebrafish yolk digestion. We will use zebrafish embryos at 0-5 days post fertilization as this time is when the yolk is digested and can be easily measured by recording the size of the yolk cell. To better characterize the effect of ulk1b knockdown, we will use immunofluorescence to visualize autophagosome formation in the yolk cell. This will give us a better understanding of the role of ulk1b in yolk digestion. With this, we hope to gain insight on autophagy mechanisms to possibly study hypoglycemia.

Comments

Jorge A. Cantu is the faculty sponsor of this project.

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Apr 19th, 9:00 AM

Autophagy Gene Ulk1B Potentially Responsible For Yolk Digestion In Zebrafish (Danio Rerio) Embryos

SU 214

Autophagy or “self-eating” is essential for a cell to maintain energy balance and overturn damaged organelles. The Ulk1b complex is a serine/threonine protein kinase responsible for autophagosome maturation and autophagy initiation. ulk1b is activated by starvation in response to glucose deficiency signals. Here, we are investigating if yolk digestion is a form autophagy carried out by the ulk1b complex. Our aim is to understand autophagy in the yolk and establish the zebrafish yolk cell as a novel system to study digestion. Within the yolk, yolk granules are present to provide nutrients needed for embryonic development. Thus, we hypothesize that if yolk digestion is a form of autophagy, knockdown of ulk1b will halt yolk digestion. To knockdown ulk1b, we will use CRISPRi, or CRISPR-mediated inhibition and study the effect on zebrafish yolk digestion. We will use zebrafish embryos at 0-5 days post fertilization as this time is when the yolk is digested and can be easily measured by recording the size of the yolk cell. To better characterize the effect of ulk1b knockdown, we will use immunofluorescence to visualize autophagosome formation in the yolk cell. This will give us a better understanding of the role of ulk1b in yolk digestion. With this, we hope to gain insight on autophagy mechanisms to possibly study hypoglycemia.