Take a look at our Research Highlight: Adriana Golding et al.
www.nature.com/articles/s41...
We highlight the work by Ghoochani et al., who generated an atlas of brain lysosomal proteins and identified SLC45A1-associated disease as a lysosomal disorder:
www.cell.com/cell/fulltex...

🔥Excited to share our new paper! We describe patients from seven independent families carrying pathogenic BLOC1S1 variants, presenting with severe neurodevelopmental disorder. These variants disrupt BLOC-1/BORC complexes. Congrats to all co-authors! 👏
authors.elsevier.com/c/1mqGAgeXHm-E

Latest preprint from our lab reports that the distinct pH of anterograde (less acidic) and retrograde (more acidic) lysosomal vesicles in the axon depends on assembly of the V1 and V0 domains of the vacuolar H+ ATPase, mediated by the metazoan RAVE complex www.biorxiv.org/content/10.6...

Job add showing the lab logo and the following text: WHAT WE OFFER Fully-funded fellowships up to five years Opportunity to start your own research program or lead ongoing projects. Large, diverse and extraordinary scientific network at the NIH/Bethesda campus. Working at NIH offers the possibility of living in a diverse, liberal and vibrant city: Washington DC Or in a calm residential area with great schools and good affordable housing: Bethesda and Rockville. WHO YOU ARE You share our enthusiasm for epigenetics, gene regulation, nuclear organization and mouse development. You have PhD-experience in one or more of the following: mouse development, mouse genetics, epigenetics, or computational biology.

🚨🚨🚨 Please repost
We are looking for postdocs to join our lab at NIH.
Apply:
www.nichd.nih.gov/research/atNICHD/Investigators/rocha/apply
Learn more about training at NIH :
www.training.nih.gov/research-tra...

BLOC-1 and BORC: Complex regulators of endolysosomal dynamics http://dlvr.it/TN9mpn

Thank you, @mishtudey.bsky.social and @cp-cellchembiol.bsky.social‬ for featuring this interview with @depaceraffa.bsky.social and Chad Williamson in connection to our article on BLOC-1 and BORC dlvr.it/TN9mpn

Job ad is here! Check it out :)

👉 New publication ahead of print from our lab: tinyurl.com/ye7pntte
We show that the protein SPG21, mutated in hereditary spastic paraplegia 21, localizes to endolysosomes via RAB7A, where it promotes mTORC1-dependent TFEB phosphorylation, reducing expression of a subset of TFEB regulated genes

New from @depaceraffa.bsky.social from our lab #NICHD #NIH in collaboration with Adeline Vanderver @childrensphila.bsky.social ‬and colleagues reporting mutations in the BLOC1S1 subunit of the BLOC-1 and BORC complexes in children with a neurodevelopmental disorder www.medrxiv.org/content/10.1...

CHIP protects lysosomes from CLN4 mutant-induced membrane damage Nature Cell Biology - Lee et al. use an aggregation-prone CLN4 mutant that causes lysosomal damage in neurons and show that in non-neurons, the ubiquitin ligase CHIP prevents CLN4-dependent...

Happy to share an exciting study from Yihong Ye’s lab at NIH, with a minor contribution from our lab: ceroid lipofuscinosis-4 (CLN4)-linked DNAJC5 mutations cause lysosomal damage as a driver of neurodegeneration in iPSC-derived neurons. CHIP safeguards lysosomes via microautophagy 👉 rdcu.be/eChof

Excited to share our new review with @depaceraffa.bsky.social‬, @saikat2025.bsky.social‬, and Chad Williamson on the BLOC-1 and BORC complexes—key regulators of endolysosomal processes and linked to several genetic diseases. #NIH #Lysosomes #RareDiseases authors.elsevier.com/a/1lg4i8jWWJ...

🚨 Exciting postdoc opportunity in @juanbonifacino.bsky.social lab!! If you have a passion for protein trafficking and neurodevelopmental disorders, and want to join a dynamic and collaborative team consider applying! Positions will be available starting in October.🍁🍂

I’m so excited to organize the #Lysosomes Subgroup at @ASCBiology 2024 meeting on Sunday, Dec. 15 at 3:15pm, Room 33B.

Lysosomes naturally lend themselves to puns. So…Don’t be 𝒃𝒂𝒔𝒊𝒄. Join us for fresh, 𝒄𝒖𝒕𝒕𝒊𝒏𝒈-edge talks and puntastic times. It will 𝒆𝒂𝒕 𝒂𝒕 𝒚𝒐𝒖 if you miss it.

This post is about a commentary that I wrote with Xin Yong about recognition of cargo vesicles by tethering factors involved in endosomes to TGN retrograde transport.

Kudos to authors Morié Ishida, Adriana Golding, @TalKerenKaplan @NICHD_NIH and our collaborators Tamas Balla @NICHD_NIH and Yan Li @NIH_NINDS! Great teamwork!

Excited to share our latest findings on how the phosphoinositide PI4P pool at the trans-Golgi network (TGN) is regulated through a SYS1-ARFRP1-ARL5-ARMH3-PI4KB pathway, in which ARMH3 (also known as C10orf76) acts as an ARL5 effector to activate PI4KB. rdcu.be/d1dZ2

Reposting @yousufakhan.bsky.social reference to a preprint demonstrating that programmed ribosomal frameshifting generates a PLEKHM2 proteoform that behaves as a constitutively active adaptor for ARL8-dependent coupling of lysosomes to kinesin-1, with collaboration from our lab tinyurl.com/mtrkzdrm