Version 1
: Received: 29 July 2024 / Approved: 30 July 2024 / Online: 30 July 2024 (10:53:56 CEST)
How to cite:
Zohud, O.; Lone, I. M.; Midlej, K.; Nashef, A.; Abu-Elnaaj, I.; Iraqi, F. A. Heterozygous Smad4 Knock out Effect on Pancreatic and Body Weight Variation in F1 Population Using Mutant and Wild Type Collaborative Cross Mice. Preprints2024, 2024072452. https://doi.org/10.20944/preprints202407.2452.v1
Zohud, O.; Lone, I. M.; Midlej, K.; Nashef, A.; Abu-Elnaaj, I.; Iraqi, F. A. Heterozygous Smad4 Knock out Effect on Pancreatic and Body Weight Variation in F1 Population Using Mutant and Wild Type Collaborative Cross Mice. Preprints 2024, 2024072452. https://doi.org/10.20944/preprints202407.2452.v1
Zohud, O.; Lone, I. M.; Midlej, K.; Nashef, A.; Abu-Elnaaj, I.; Iraqi, F. A. Heterozygous Smad4 Knock out Effect on Pancreatic and Body Weight Variation in F1 Population Using Mutant and Wild Type Collaborative Cross Mice. Preprints2024, 2024072452. https://doi.org/10.20944/preprints202407.2452.v1
APA Style
Zohud, O., Lone, I. M., Midlej, K., Nashef, A., Abu-Elnaaj, I., & Iraqi, F. A. (2024). Heterozygous <i>Smad4</i> Knock out Effect on Pancreatic and Body Weight Variation in F1 Population Using Mutant and Wild Type Collaborative Cross Mice. Preprints. https://doi.org/10.20944/preprints202407.2452.v1
Chicago/Turabian Style
Zohud, O., Imad Abu-Elnaaj and Fuad A. Iraqi. 2024 "Heterozygous <i>Smad4</i> Knock out Effect on Pancreatic and Body Weight Variation in F1 Population Using Mutant and Wild Type Collaborative Cross Mice" Preprints. https://doi.org/10.20944/preprints202407.2452.v1
Abstract
Background: Smad4, a critical tumor suppressor gene, plays a significant role in pancreatic biology and tumorigenesis. Genetic background and sex are known to influence phenotypic outcomes, but their impact on pancreatic weight in Smad4-deficient mice remains unclear. This study investigates the impact of Smad4 deficiency on pancreatic weight in F1 mice from diverse Collaborative Cross (CC) lines, focusing on the influence of genetic background and sex. Methods: F1 mice were generated by crossbreeding female CC mice with C57BL/6J-Smad4tm1Mak males. Genotyping confirmed the presence of Smad4 knockout alleles. Mice were housed under standard conditions, euthanized at 80 weeks, and their pancreatic weights were measured, adjusted for body weight, and analyzed for effects of Smad4 deficiency, sex, and genetic background. Results: The overall population of F1 mice showed a slight but non-significant increase in adjusted pancreatic weights in heterozygous knockout mice compared to wild-type mice. Sex-specific analysis revealed no significant difference in males but a significant increase in adjusted pancreatic weights in heterozygous knockout females. Genetic background analysis showed that lines CC018 and CC025 substantially increased adjusted pancreatic weights in heterozygous knockout mice. In contrast, other lines showed no significant difference or varied non-significant changes. The interplay between genetic background and sex further influenced these outcomes. Conclusion: Smad4 deficiency affects pancreatic weight in a manner significantly modulated by genetic background and sex. This study highlights the necessity of considering these factors in genetic research and therapeutic development, demonstrating the value of the Collaborative cross-mouse population in dissecting complex genetic interactions.
Keywords
Smad4; pancreatic weight; genetic background; sex differences; Collaborative Cross; F1 mice; genetic modifiers; tumor suppressor gene
Subject
Biology and Life Sciences, Other
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
