Table S1: Primer sets used for cloning of N and C-V5 aromatase mutants from Aromatase Acetylation Patterns and Altered Activity in Response to Sirtuin Inhibition

Supplementary Table 1: Primer sets used in cloning of aromatase into pcDNA3.1+ and those used to amplify V5-tagged aromatase in a pool of RNA and their expected DNA product size.</p

Figure S2 from Aromatase Acetylation Patterns and Altered Activity in Response to Sirtuin Inhibition

Aromatase peptides are acetylated in MCF-7 cells.</p

Figure S1 from Aromatase Acetylation Patterns and Altered Activity in Response to Sirtuin Inhibition

Expression of endogenous aromatase protein and exogenous aromatase constructs in different cell lines and their effect on estradiol levels</p

Figure S3 from Aromatase Acetylation Patterns and Altered Activity in Response to Sirtuin Inhibition

V5-tagged aromatase protein colocalizes with endoplasmic reticulum marker calnexin in stably transfected HEK293 cells.</p

Table S4: Acetylated lysines on aromatase peptides identified by LC-MS/MS analysis in MCF-7 cells. from Aromatase Acetylation Patterns and Altered Activity in Response to Sirtuin Inhibition

Supplementary Table 4: Detailed LC-MS/MS data of acetylated aromatase protein. Table showing the location of basally (clear) and SIRT-1 inhibitor IV induced (highlighted) acetylation of aromatase peptides from MCF-7 cells under conventional (20% O2) and physiological oxygen (2.5% O2) conditions.</p

Table S3:Primer sets used for site-directed mutagenesis to generate K108 and K440 aromatase mutants from Aromatase Acetylation Patterns and Altered Activity in Response to Sirtuin Inhibition

Supplementary Table 3: Primer sets used in the generation of aromatase mutants during site directed mutagenesis.</p

Table S2:SIRT-1 siRNA sequence and gene location from Aromatase Acetylation Patterns and Altered Activity in Response to Sirtuin Inhibition

Supplementary Table 2: siGENOME SMARTpool, Human SIRT1 siRNA sequence and exon location in the gene.</p

Catastrophic consequences of Hltf-deletion from pancreatic β cells during development.

Recruitment of NK cells expressing Prf1-GzmA—triggered by the Hmgb1-RAGE axis in response to impaired DNA-damage repair—perpetuated DNA damage and selective loss of pancreatic β cells. Created with Biorender.com.</p

Statistics for spatial transcriptomics outcome for Visium_FFPE_Mouse_Pancreas in ID β <i>Hltf</i>-KO (Sample ID, A and B) and IC β <i>Hltf</i>-KO (Sample ID, C and D).

Statistics for spatial transcriptomics outcome for Visium_FFPE_Mouse_Pancreas in ID β Hltf-KO (Sample ID, A and B) and IC β Hltf-KO (Sample ID, C and D).</p

Differential γH2Ax pan-staining and TUNEL assay.

Abundant γH2Ax in β cells from IC β Hltf KO mice (A) compared to minimal immunostaining in β cells from ID β Hltf KO mice (B). Two-types of γH2Ax pan-staining are evident. β cells from IC β Hltf KO mice have apoptotic rings and the β cells from ID β Hltf KO mice have limited pan-nuclear staining of the entire nucleus. Results from the terminal deoxynuceotidyl transferase dUTP nick-end labeling (TUNEL) assay (C), which detects β cell death-associated DNA fragmentation (3’-OH termini), indicates the amount of DNA damage is more than the targeted β cells can efficiently repair when the animals are IC. Cell-death in IC Hltf +/+ controls and ID β Hltf KO mice was negligible. A positive mouse testis control (D) was included because apoptosis is an important component of normal spermatogenesis.</p