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SOHLH1 and NOBOX are oocyte‐expressed transcription factors with critical roles in ovary development and fertility. In mice, Sohlh1 and Nobox are essential for fertility through their regulation of the oocyte transcriptional network and cross‐talk to somatic cells. Sumoylation is a posttranslational modification that regulates transcription factor function, and we previously showed that mouse oocytes deficient for sumoylation had an altered transcriptional landscape that included significant changes in NOBOX target genes. Here, we show that mouse SOHLH1 is modified by SUMO2/3 at lysine 345 and mutation of this residue alters SOHLH1 nuclear to cytoplasmic localization. In NOBOX, we identify a non‐consensus SUMO site, K97, that eliminates NOBOX mono‐SUMO2/3 conjugation, while a point mutation at K125 had no effect on NOBOX sumoylation. However, NOBOXK97R/K125R double mutants showed loss of mono‐SUMO2/3 and altered higher molecular weight modifications, suggesting cooperation between these lysine's. NOBOXK97R and NOBOXK97R/K125R differentially regulated NOBOX promoter targets, with increased activity on the Gdf9 promoter, but no effect on the Pou5f1 promoter. These data implicate sumoylation as a novel regulatory mechanism for SOHLH1 and NOBOX, which may prove useful in refining their roles during oogenesis as well as their function during reprogramming to generate de novo germ cells.

Patients with NASH were identified (ICD-10 diagnosis code K7581). Patients were split into elective and non-elective cohorts. Length of stay and cost estimates were evaluated. Cost estimates were calculated using total charges for hospital services using hospital specific cost-to-charge ratios based on all-payer inpatient costs derived from the Centers for Medicare and Medicaid Services (CMS). Statistical analysis was performed with SPSS version 25 (2017 IBM Corporation, Armonk NY). Results: 223 patients admitted for non-elective TIPS were identified; of these 33 patients carried a diagnosis of NASH. Length of stay was significantly higher for patients admitted for non-elective TIPS with NASH (13.8 versus 9.4 days, P ¼ 0.008). Estimated cost for an inpatient admission for patients with NASH was not significantly different than those with other causes of cirrhosis ($50,506.94 vs $46,137.01, P ¼ 0.32). Risk of mortality for patients with NASH between the two groups (OR 0.17, 95% CI 0.02 -1.32).103 patients were admitted for elective TIPS; of these 19 patients carried a diagnosis of NASH. In the elective group there was no difference for patients with NASH versus those with other causes of cirrhosis in length of stay (2.3 vs 3.6 days, P ¼ 0.174), estimated cost (14,794.56 vs 20,744.55, P ¼ 0.110), or mortality (OR -0.12, 95% CI -0.06 -0.038). Conclusions: Patients with NASH admitted for non-elective TIPS experience statistically significantly longer hospital stays than those admitted with other causes of cirrhosis. While length of stay and estimated cost are higher in the setting of non-elective versus elective TIPS admissions in both groups, there is no difference in length of stay for patients with NASH versus those with other causes of cirrhosis admitted for elective TIPS placement. This suggests that extended length of stay after non-elective TIPS in patients with NASH may be mitigated with planned admission for TIPS placement.