Biology subjects

Zhang, Q.-H.

Publications and source records attributed to Zhang, Q.-H..

3 recordsLinked to original sources

bioRxiv2024

Does What You Eat Affect How You Mate? Disentangling the Interactions Between Diet-Induced Phenotypic Plasticity and Adult Reproductive Strategies in Black Soldier Flies.

Phenotypic plasticity enables organisms to response to environmental variations by generating a range of phenotypes from a single genotype. In holometabolous insects, traits that influence larval plasticity may hold relevance for adult life history strategies. We present a comprehensive investigation into phenotypic plasticity in black soldier flies, a species known for its efficient waste-to-biomass conversion in the larval stage. Here, we document adult sex-specific plastic responses and reproductive strategies shaped by larval diets. We examined traits including adult body size, reproductive organ development, sperm length, mating behaviours, egg production and other life history parameters across different treatments. Our findings reveal notable sex-specific differences in phenotypic plasticity, with females showing increased plasticity in reproductive investment. Furthermore, males and females differed starkly in allometric growth and weight ratio of reproductive organs. Diets that facilitated longer male lifespans also prompted earlier male emergence suggesting an interplay between lifespan and degree of protandry. This maximizes the overlap of male and female lifespans, thereby enhancing mating success in diverse environmental conditions. Our results reveal plastic responses in mating behaviours, where diets producing smaller adults, smaller reproductive organs, and shorter sperm correlated with significantly enhanced mating effort and performance. This study highlights the complex interactions between nutrition, development, and reproductive strategies, and has significant implications for the insect bioconversion industries.

evolutionary biology↗

bioRxiv2023

Fertility is compromised after oocyte-specific deletion of Katanin A-subunit, Katna1, but not Katnal1

Katanins are microtubule severing enzymes that play roles in shaping diverse microtubule-based structures during all cell cycle stages. To address the role of katanin A-subunits in mammalian oocytes, we have used the Zp3-CreLox approach to specifically delete katanin A1 (Katna1) and katanin A-like 1 (Katnal1) from the start of oocyte growth in mice. Here, we show that Katnal1 is not required for normal female fertility, but that deletion of Katna1 causes a 50% decrease in fertility. Further investigation in Katna1-/- oocytes revealed no effect on MI spindle morphology but a significant effect on the morphology of MII spindles. This was accompanied by a decreased rate of fertilisation. Resultant Katna1+/- heterozygous embryos that reached the 2-cell stage developed at normal rates to the blastocyst stage. Diploid homozygous parthenotes derived from Katna1-/- oocytes revealed a reduced rate of blastocyst formation, decreased cell number and increased nuclear size. The ability of the paternal allele to rescue preimplantation development suggests the origin of the decrease in the fertility of conditional Katna1-/- mice lies in abnormalities arising in the egg to embryo transition prior to embryonic genome activation.

developmental biology↗

bioRxiv2022

Transient Polycomb activity represses developmental genes in growing oocytes.

BackgroundNon-genetic disease inheritance and offspring phenotype is substantially influenced by germline epigenetic programming, including genomic imprinting. Loss of Polycomb Repressive Complex 2 (PRC2) function in oocytes causes non-genetically inherited effects on offspring, including embryonic growth restriction followed by post-natal offspring overgrowth. While PRC2 dependent non-canonical imprinting is likely to contribute, less is known about germline epigenetic programming of non-imprinted genes during oocyte growth. In addition, de novo germline mutations in genes encoding PRC2 lead to overgrowth syndromes in human patients, but the extent to which PRC2 activity is conserved in human oocytes is poorly understood. ResultsIn this study we identify a discrete period of early oocyte growth during which PRC2 is expressed in mouse growing oocytes. Deletion of Eed during this window led to the de-repression of 343 genes. A high proportion of these were developmental regulators, and the vast majority were not imprinted genes. Many of the de-repressed genes were also marked by the PRC2-dependent epigenetic modification histone 3 lysine 27 trimethylation (H3K27me3) in primary-secondary mouse oocytes, at a time concurrent with PRC2 expression. In addition, we found H3K27me3 was also enriched on many of these genes by the germinal vesicle (GV) stage in human oocytes, strongly indicating that this PRC2 function is conserved in the human germline. However, while the 343 genes were de-repressed in mouse oocytes lacking EED, they were not de-repressed in pre-implantation embryos and lost H3K27me3 during pre-implantation development. This implies that H3K27me3 is a transient feature that represses a wide range of genes in oocytes. ConclusionsTogether, these data indicate that EED has spatially and temporally distinct functions in the female germline to repress a wide range of developmentally important genes, and that this activity is conserved in the mouse and human germlines.

developmental biology↗