Thank you!!!! 🪰💙

To find out more about their work, we spoke to first author Danielle Spitzer @dspitzer.bsky.social and corresponding author Iswar Hariharan, Professor at the University of California, Berkeley, USA:

journals.biologists.com/dev/article/...

For some more behind-the-scenes on this paper, check out this interview with me and Iswar! (8/8) journals.biologists.com/dev/article/...

A HUGE thanks to my co-authors: Anthony Rodríguez-Vargas helped with the genetic screen, and William Sun conducted many key experiments after I graduated (including the one showing that ed- discs secrete Ilp8, all of S5 and S7, and much of S6). Science is a team sport! (7/8)

We propose a revised model of how Ed functions in growth regulation, emphasizing that context matters. Also, Ed is known to affect EGFR, Notch, Hippo, cell adhesion, and membrane trafficking...so mutant phenotypes may involve complex effects on multiple pathways/processes at once (6/8)

Although ed- clones are eliminated, ed- compartments/organs overgrow. There are still high levels of apoptosis in these tissues, but the organs keep growing for an extended period of time (this involves secretion of Ilp8 which delays pupariation) and the organs can eventually become very large (5/8)

It has been proposed that Ed functions in the Hippo pathway to restrict expression of pro-growth Yki target genes. However, we found that Ed loss led to reduced expression of some Yki target genes in ed- clones! We sometimes observed a border effect with increased expression in WT neighbors (4/8)

When ed- clones are generated in the presence of WT cells, mutant clones are eliminated. This is because ed- cells have elevated apoptosis rates and reduced levels of Diap1. This is especially pronounced at clone borders, suggesting that competition with WT cells may be involved (3/8)

We conducted a screen to identify adhesion molecules that regulate the growth of mutant clones. We focused on Ed since reducing its function in mosaics led to clone undergrowth/elimination, but previous work suggests that these mutant cells should overgrow. Hmmmmmm…… (2/8)

Important to note that this work (and nearly all US based biomedical research) would not have been possible without funding from the #NIH.

There’s an activation energy barrier to prepping a new mini-lesson on an unfamiliar topic on short notice, so happy to share my slides with others who might be considering doing this in their classroom too. 4/4

I was nervous I would miss something (e.g. what the heck is going on with the DEI EO? Did I explain indirects right? Has the situation changed again?) but ultimately decided that if I—a PhD scientist whose training was funded by federal grant $—was confused, it must be way worse for my students. 3/4

I focused my slides on why research matters to my physiology students (mostly bioscience majors pursuing health professions) and how the recent changes impact Pitt. 2/4

Yes, will do!