Catarina Colmatti Bromatti and Danielle Farinella to Speak

Catarina Colmatti Bromatti and Danielle Farinella -- Levin Lab

Title:

Dumpy regulation across space and time in posterior lobe development (Catarina)

Investigating the molecular interactions of host-pathogen co-evolution in Legionella pneumophila and Dictyostelium discoideum (Danielle)

Abstract:

Catarina: The evolution of complex new structures, so-called “morphological novelties”, is a topic of intense study in the field of evolutionary developmental biology. Gene regulatory networks that control developmental expression are critical to explaining how new structures deploy genes to achieve their unique morphological features. In particular, we need examples which explain how genes that execute new and essential functions in the new tissue have derived their expression at the molecular level. Here, I use Drosophila melanogaster as a model organism to study a recently evolved novel genital structure called the posterior lobe. Previous work has found that the posterior lobe required the recruitment of apical extracellular matrix (aECM) during its developmental evolution. The protein Dumpy is present in the aECM, and disruption of dumpy causes the posterior lobe to almost disappear completely. In my project, I am investigating how dumpy gained posterior lobe-associated regulation. I have identified a candidate enhancer sufficient to drive reporter expression in the cells of the posterior lobe. I will use CRISPR mediated deletions to test the necessity of this enhancer. Moreover, comparing the homologous sequences of this enhancer between lobed species and non-lobed species will reveal whether it was an ancestral enhancer or newly evolved to have posterior lobe activity. Finally, I am interested in exploring whether this enhancer is also functional in other tissues. A shared regulatory role in another tissue would indicate that this enhancer, and potentially an entire genetic network might have been redeployed from a conserved tissue to the posterior lobe, facilitating the origin of this novelty. Thus, Identifying the enhancers of dumpy and their evolutionary history provides a much needed window into how a process involving dozens if not hundreds of genes may have occurred.

Danielle: It is estimated that there are 1 trillion species of prokaryotes on Earth. These species are constantly evolving. Some of them will evolve into human pathogens. Bacteria that replicate in amoeboid hosts can enter an “arms race” in which, over many evolutionary cycles, bacteria can evolve to evade the amoebas’ innate immune system. This selective pressure can facilitate evolution into a human pathogen. To study how this co-evolution alters the molecular weaponry of bacteria, we will investigate how co-evolution between Dictyostelium discoideum (Dd) and Legionella pneumophila (Lp) facilitated the evolution of Lp’s ability to infect human macrophages. First, we will investigate which Lp genes are necessary for infection and replication within Dd cells. These genes (called ‘effectors’) will be identified by passaging an Lp Tn-seq transposon insertion library through Dd cells. This library will also be passaged through immunocompromised Dd to pair Lp effectors with Dd immune genes. Preliminary data has shown the Type II Secretion System (T2SS) of Lp to be critical for Dd infection. To test which T2SS genes are important for infection, we will generate knockouts of T2SS genes and examine their ability to replicate in Dd. For any genes that promote Dd infection, we will identify homologs and compare the homologs’ ability to promote infection. By doing this comparison, we can identify residues needed for the gene’s functionality. By utilizing the Tn-seq screen and exploring the mechanisms of the T2SS virulence genes, we can begin to identify the faces of evolutionary conflict in the context of pathogenesis. 

Friday, September 9th, 2022

A219B Langley Hall

12:00 PM

Date

09 Sep 2022

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Graduate Student Presentations

Location

A219B Langley Hall