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Gilbert, M. B.

Publications and source records attributed to Gilbert, M. B..

3 recordsLinked to original sources

Expanding the HIF-2α proteomic interactome with TurboID proximity labeling.

The transcription factor HIF2 is a central regulator of cellular adaptation to hypoxia, orchestrating gene expression programs that control angiogenesis, erythropoiesis, and metabolic reprogramming, and is famously overexpressed in cancers such as clear cell Renal Cell Carcinoma (ccRCC). While the gene targets of HIF2 have been extensively characterized, the composition and dynamics of its protein interaction network remain less well defined. In this study, we sought to systematically characterize proteins associated with HIF2 using two distinct proteomic approaches, enabling the identification of both stable binding partners and transient or indirect interactors. We integrated affinity purification mass spectrometry with proximity labeling strategies, thus expanding the existing interactome of HIF2 to include uniquely identified proteins and complexes such as members of the nuclear pore complex. Across both immunoprecipitation mass spectrometry (IP MS) and TurboID MS, we identified 888 and 1,048 proteins, respectively. We applied stringent filtering criteria to refine both datatsets, yielding a dataset of 329 HIF2 interacting proteins, approximately 75% of which have yet to be documented as HIF2 interactors. We queried this set across publicly available cancer genomics and proteomics datasets and detected expression of our interactors in breast cancer and ccRCC tumor proteomes. These findings led us to identify GRHL2 and KIF4A as proteomic interactors that contribute to poor patient survival in breast cancer. Taken together, we herein provide a comprehensive resource of HIF2 interacting proteins which provide insights into the mechanisms by which HIF2 drives disease progression.

biochemistry↗

Neuropeptides specify and reprogram division of labor in the leafcutter ant Atta cephalotes

Social insects offer powerful models to investigate the mechanistic foundation of elaborate individual behaviors comprising a cooperative community. Workers of the leafcutter ant genus Atta provide an extreme example of behavioral segregation among many phenotypically distinct worker types. We utilize the complex worker system of Atta cephalotes to test the molecular underpinnings of behavioral programming and, in particular, the extent of plasticity to reprogramming. We identify specific neuropeptides as mediators of worker division of labor in A. cephalotes, finding two neuropeptides associated with characteristic behaviors of leafcutting and of brood care. Manipulation via genetic knockdown or by injection of these neuropeptides led to stark loss or gain of each behavior and to transcriptomic shifts in the predicted direction, that is, towards gene pathways expressed in the natural caste. We also compare specific A. cephalotes worker transcriptomes with those of orthologous workers of the eusocial mammal, the naked mole rat H. gaber, revealing global similarities between caste-biased expression and link to specific roles of our studied neuropeptides in ants. This work underscores the essential function of neuropeptides in establishing complex social behavior and a remarkable plasticity among individual behavioral types.

molecular biology↗

Distinct H3K9me3 heterochromatin maintenance dynamics govern different gene programs and repeats in pluripotent cells

H3K9me3-heterochromatin, established by lysine methyltransferases (KMTs) and compacted by HP1 isoforms, represses alternative lineage genes and DNA repeats. Our understanding of H3K9me3-heterochromatin stability is presently limited to individual domains and DNA repeats. We engineered Suv39h2 KO mouse embryonic stem cells to degrade remaining two H3K9me3- KMTs within one hour and found that both passive dilution and active removal contribute to H3K9me3 decay within 12-24 hours. We discovered four different H3K9me3 decay rates across the genome and chromatin features and transcription factor binding patterns that predict the stability classes. A "binary switch" governs heterochromatin compaction, with HP1 rapidly dissociating from heterochromatin upon KMTs depletion and a particular threshold level of HP1 limiting pioneer factor binding, chromatin opening, and exit from pluripotency within 12 hr. Unexpectedly, receding H3K9me3 domains unearth residual HP1{beta} peaks enriched with heterochromatin-inducing proteins. Our findings reveal distinct H3K9me3-heterochromatin maintenance dynamics governing gene networks and repeats that together safeguard pluripotency.

cell biology↗