Experimental study on color and texture as cues for plastic debris ingestion by captive sea turtles.

Sea turtles face considerable risks from ingesting marine debris. They are primarily visual feeders, so color may be important for identifying food suitability or enhancing prey detection. Here, we investigated the impacts of color and texture on foraging behavior in relation to plastic consumption. We experimentally assessed the influences of color and texture as attractors for sea turtles using edible jellyfish. The findings showed that the colors of objects significantly affected selective preferences, as evidenced by different behaviors by sea turtles in response to different colors. They exhibited diet-related selectivity toward colors similar to common aquarium food, and texture had a significant impact on complete ingestion. The results suggest that plastic resembling natural prey is more likely ingested. Also, sea turtles were attracted by the color yellow, suggesting that visually distinctive items can attract them. Our results provide fundamental knowledge, helping mitigate the effects of plastic pollution on wildlife.

Imperfect mimicry of host begging calls by a brood parasitic cuckoo: a cue for nestling rejection by hosts?

Coevolutionary interactions between avian brood parasites and their hosts often lead to the evolution of discrimination and rejection of parasite eggs or chicks by hosts based on visual cues, and the evolution of visual mimicry of host eggs or chicks by brood parasites. Hosts may also base rejection of brood parasite nestlings on vocal cues, which would in turn select for mimicry of host begging calls in brood parasite chicks. In cuckoos that exploit multiple hosts with different begging calls, call structure may be plastic, allowing nestlings to modify their calls to match those of their various hosts, or fixed, in which case we would predict either imperfect mimicry or divergence of the species into host-specific lineages. In our study of the little bronze-cuckoo (LBC) Chalcites minutillus and its primary host, the large-billed gerygone Gerygone magnirostris, we tested whether: (1) hosts use nestling vocalizations as a cue to discriminate cuckoo chicks; (2) cuckoo nestlings mimic the host begging calls throughout the nestling period; and (3) the cuckoo begging calls are plastic, thereby facilitating mimicry of the calls of different hosts. We found that the begging calls of LBCs are most similar to their gerygone hosts shortly after hatching (when rejection by hosts typically occurs) but become less similar as cuckoo chicks get older. Begging call structure may be used as a cue for rejection by hosts, and these results are consistent with gerygone defenses selecting for age-specific vocal mimicry in cuckoo chicks. We found no evidence that LBC begging calls were plastic.

True recognition of nestlings by hosts selects for mimetic cuckoo chicks.

Brood parasitic cuckoos lay their eggs in other birds' nests, whereafter the young cuckoo hatches, ejects its nest-mates and monopolizes the care of the host parents. Theory predicts that hosts should not evolve to recognize and reject cuckoo chicks via imprinting because of the risk of mistakenly imprinting on a cuckoo chick in their first brood and thereafter always rejecting their own chicks. However, recent studies have revealed that some hosts do reject cuckoo chicks from the nest, indicating that these hosts' recognition systems either do not rely on first brood imprinting, or use cues that are independent of chick phenotype. Here, we investigate the proximate mechanisms of chick rejection behaviour in the large-billed gerygone (Gerygone magnirostris), a host of the little bronze-cuckoo (Chalcites minutillus). We find that gerygones use true template-based recognition based on at least one visual chick trait (the number of hatchling down-feathers), and that this is further mediated by experience of adult cuckoos at the nest during egg-laying. Given the theoretical constraints of acquiring recognition templates via imprinting, gerygones must possess a template of own-chick appearance that is largely innate. This true recognition has facilitated the evolution of very rapid hatchling rejection and, in turn, striking visual mimicry of host young by little bronze-cuckoo chicks.

Role of MIZ-1 in AMELX gene expression.

Amelogenin (AMELX) is the main component of the developing tooth enamel matrix and is essential for enamel thickness and structure. However, little is known about its transcriptional regulation. Using gene expression analysis, we found that MIZ-1, a potent transcriptional activator of CDKN1A, is expressed during odontoblastic differentiation of hDPSCs (human dental pulp stem cells), and is essential for odontoblast differentiation and mineralization. We also investigated how MIZ-1 regulates gene expression of AMELX. Oligonucleotide-pull down assays showed that MIZ-1 binds to an MRE (MIZ-1 binding element) of the AMELX proximal promoter region (bp, -170 to -25). Combined, our ChIP, transient transcription assays, and promoter mutagenesis revealed that MIZ-1 directly binds to the MRE of the Amelx promoter recruits p300 and induces Amelx gene transcription. Finally, we show that the zinc finger protein MIZ-1 is an essential transcriptional activator of Amelx, which is critical in odontogenesis and matrix mineralization in the developing tooth.

Spatial patterns, ecological niches, and interspecific competition of avian brood parasites: inferring from a case study of Korea.

Since obligate avian brood parasites depend completely on the effort of other host species for rearing their progeny, the availability of hosts will be a critical resource for their life history. Circumstantial evidence suggests that intense competition for host species may exist not only within but also between species. So far, however, few studies have demonstrated whether the interspecific competition really occurs in the system of avian brood parasitism and how the nature of brood parasitism is related to their niche evolution. Using the occurrence data of five avian brood parasites from two sources of nationwide bird surveys in South Korea and publically available environmental/climatic data, we identified their distribution patterns and ecological niches, and applied species distribution modeling to infer the effect of interspecific competition on their spatial distribution. We found that the distribution patterns of five avian brood parasites could be characterized by altitude and climatic conditions, but overall their spatial ranges and ecological niches extensively overlapped with each other. We also found that the predicted distribution areas of each species were generally comparable to the realized distribution areas, and the numbers of individuals in areas where multiple species were predicted to coexist showed positive relationships among species. In conclusion, despite following different coevolutionary trajectories to adapt to their respect host species, five species of avian brood parasites breeding in South Korea occupied broadly similar ecological niches, implying that they tend to conserve ancestral preferences for ecological conditions. Furthermore, our results indicated that contrary to expectation interspecific competition for host availability between avian brood parasites seemed to be trivial, and thus, play little role in shaping their spatial distributions and ecological niches. Future studies, including the complete ranges of avian brood parasites and ecological niches of host species, will be worthwhile to further elucidate these issues.

Two ZNF509 (ZBTB49) isoforms induce cell-cycle arrest by activating transcription of p21/CDKN1A and RB upon exposure to genotoxic stress.

ZNF509 is unique among POK family proteins in that four isoforms are generated by alternative splicing. Short ZNF509 (ZNF509S1, -S2 and -S3) isoforms contain one or two out of the seven zinc-fingers contained in long ZNF509 (ZNF509L). Here, we investigated the functions of ZNF509 isoforms in response to DNA damage, showing isoforms to be induced by p53. Intriguingly, to inhibit proliferation of HCT116 and HEK293 cells, we found that ZNF509L activates p21/CDKN1A transcription, while ZNF509S1 induces RB. ZNF509L binds to the p21/CDKN1A promoter either alone or by interacting with MIZ-1 to recruit the co-activator p300 to activate p21/CDKN1A transcription. In contrast, ZNF509S1 binds to the distal RB promoter to interact and interfere with the MIZF repressor, resulting in derepression and transcription of RB. Immunohistochemical analysis revealed that ZNF509 is highly expressed in normal epithelial cells, but was completely repressed in tumor tissues of the colon, lung and skin, indicating a possible role as a tumor suppressor.