Exploring the Genetic Background of the Differences in Nest-Building Behavior in European Rabbit
- Once a day, nursing and absentee mothering make the wild rabbit (Oryctolagus cuniculus) an ideal model animal for measuring differences in maternal behavior. Behavioral events and their hormonal regulation leading to parturition are well documented; however, the genetic background behind individual differences in this complex process is unknown.
- Decreased progesterone hormone level and the reduction of progesterone receptor activity are crucial to initiating the collection of nest material. The progesterone receptor gene is a likely candidate affecting nest-building behavior. In addition to several known point mutations in the progesterone receptor gene of the European wild rabbit, we have found a new mutation in the promoter region of the gene at 2682 T > C.
- Although this new single nucleotide polymorphism (SNP) was not involved in the formation of the nest-building behavior, an SNP (2464G > A) already described in the promoter region showed an association with individual differences in the initiation of hay carrying. The distribution of this SNP delivered an opposite result compared to domestic rabbits.
- Genotype (GG) with high uterine capacity was most frequent; the hereditary value of the trait was h2 = 0.10. Thus, progesterone receptor gene polymorphism may manifest in individual differences affecting breeding success in this species.

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Examination of genetic and pharmacological tools to study the proteasomal deubiquitinating enzyme USP14 in the nervous system
Strategies for enhancing protein degradation have been proposed for treating neurological diseases associated with a decline in proteasome activity. A proteasomal deubiquitinating enzyme that controls substrate entry into proteasomes, ubiquitin-specific protease 14 (USP14), is an attractive candidate for therapies that modulate proteasome activity.
This report tests the validity of genetic and pharmacological tools to study USP14’s role in regulating protein abundance. Although previous studies implicated USP14 in the degradation of MAPT, TARDBP, and PRNP, the levels of these proteins were similar in our neurons cultured from wild type and USP14-deficient mice. Neither loss nor overexpression of USP14 affected the levels of these proteins in mice, implying that modifying the amount of USP14 is not sufficient to alter their steady-state levels.
However, neuronal overexpression of a catalytic mutant of USP14 showed that manipulating USP14’s ubiquitin-hydrolase activity altered the levels of specific proteins in vivo. Although pharmacological inhibitors of USP14’s ubiquitin-hydrolase activity reduced MAPT, TARDBP, and PRNP in culture, the effect was similar in wild type and USP14-deficient neurons, thus impacting their use for specifically evaluating USP14 in a therapeutic manner.
While examining how targeting USP14 may affect other proteins in vivo, this report showed that FASN, RELA, CTNNB1, and SNAP23 are reduced in USP14-deficient mice; however, loss of USP14 differentially altered the levels of these proteins in the liver and brain. As such, it is critical to more thoroughly examine how inhibiting USP14 alters protein abundance to determine if targeting USP14 will be a beneficial strategy for treating neurodegenerative diseases.
Construction of Gossypiumbarbadense Mutant Library Provides Genetic Resources for Cotton Germplasm Improvement
Allotetraploid cotton (Gossypium hirsutum and Gossypium barbadense) are cultivated worldwide for its white fiber. For centuries, conventional breeding approaches increase cotton yield at the cost of extensive erosion of natural genetic variability. Sea Island cotton (G. barbadense) is known for its superior fiber quality, but show poor adaptability as compared to Upland cotton.
Here, in this study, we use ethylmethanesulfonate (EMS) as a mutagenic agent to induce genome-wide point mutations to improve the current germplasm resources of Sea Island cotton and develop diverse breeding lines with improved adaptability and excellent economic traits. We determined the optimal EMS experimental procedure suitable for construction of cotton mutant library.
At M6 generation, mutant library comprised of lines with distinguished phenotypes of the plant architecture, leaf, flower, boll, and fiber. Genome-wide analysis of SNP distribution and density in yellow leaf mutant reflected the better quality of mutant library. Reduced photosynthetic efficiency and transmission electron microscopy of yellow leaf mutants revealed the effect of induced mutations at physiological and cellular level. Our mutant collection will serve as the valuable resource for basic research on cotton functional genomics, as well as cotton breeding.
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