Social monogamy evolves in association with biparental care. However, males who tend to pursue multiple mating are expected to place less value on established partnerships, whereas females do the opposite to ensure males' participation in rearing offspring. Accordingly, selection is expected to favor paired females to behave aggressively towards females that approach their social mates. For species with long-term partnerships, female-female aggression commonly observed during the breeding period should also occur in the non-breeding period. We look at whether these expectations are held up by conducting a field experiment in Tibetan ground tits Pseudopodoces humilis, a cooperatively breeding bird that has lifetime monogamy and forms new pair bonds in winter. Paired but not unpaired females were more aggressive towards the same-sex than towards opposite-sex intruders experimentally introduced into the winter group territory, an indication that paired females may be protecting partnerships. Both paired and unpaired males, on the other hand, displayed aggression almost equally against intruders of both sexes, indicating a likely function in territory defense. Our work provides the first evidence for the female's role in maintaining long-term monogamy during the non-breeding period in birds, and contributes to the recent progress regarding intrasexual competition between females as a component of sexual selection.

Cervical cancer (CC) is the most common malignancy of the female reproductive system, among which cervical squamous cell carcinoma (CESC) is the most common type. The demethylase ALKBH5 has been previously revealed to be downregulated in CC tissue. N6 methyladenine (m6A) is the most common modification in eukaryotic RNAs and is involved in modulating tumour progression. Therefore, we attempted to clarify the ALKBH5 role and mechanism underlying CESC progression.In CESC, patient tissue and control tissue m6A levels were measured. Reverse transcription quantitative real-time polymerase chain reaction, western blotting and immunochemistry were used to measure ALKBH5 levels. A correlation between CESC patient survival and ALKBH5 levels was evaluated. Wound healing, transwell and colony formation assays were used to detect CESC cellular behaviours. Corresponding kits and BODIPY staining were used to detect CESC lipid metabolism. Bioinformatics, immunoprecipitation, RNA pulldown and RNA immunoprecipitation assays as well as half-life measurements were used to assess the association and mechanism of ALKBH5 with silent mating type information regulation 2 homologue 3 (SIRT3), acetyl-CoA carboxylase 1 (ACC1) and insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1). The m6A demethylase ALKBH5 was depleted in CESC tissue and cells, and a low level of ALKBH5 predicted an unfavourable prognosis in CESC patients. ALKBH5 overexpression suppressed CESC growth and lipid metabolism in vitro and CESC tumour growth in vivo, and ACC1 overexpression rescued these changes. ALKBH5 downregulated ACC1 levels in CESC cells by facilitating SIRT3 methylation to repress ACC1 deacetylation. ALKBH5 destabilized SIRT3 to downregulate SIRT3 levels in CESCs in an m6A-IGF2BP1-dependent manner.ALKBH5 demethylates and destabilizes SIRT3 in an m6A-IGF2BP1-dependent manner, repressing CESC growth, lipid metabolism and tumorigenesis by downregulating ACC1.

No abstract

No abstract

No abstract