
本文探討 RNA 結合抗終止子在革蘭氏陽性和革蘭氏陰性細菌致病性中的調控作用，強調其作為潛在藥物靶點的重要性。


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細菌致病性中-rna-結合抗終止子的調控作用


細菌致病性中 RNA 結合抗終止子的調控作用


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生物系統的配置空間可以快速擴張，這可能會對宇宙的信息內容產生重大影響。


生物宇宙學-邁向一門新科學的誕生


生物宇宙學：邁向一門新科學的誕生



短熱休克因子A2、A4c和B1是新型的熱休克因子,通過結合新的熱調控元件(HRE)來負調控極端高溫耐受性。使用短熱休克因子A2作為代表,我們進一步揭示了短熱休克因子如何防止由於HSP17.6B過表達導致的典型熱休克反應過度激活,從而維持適當的生長。


Cells prevent heat damage through a highly conserved canonical heat stress response (HSR) in which heat shock factors (HSFs) bind heat shock elements (HSEs) to activate heat shock proteins (HSPs). Plants generate short HSFs that originate from HSF splicing variants, but little is known about S-HSFs. Although an enhanced canonical HSR confers thermotolerance, its hyperactivation inhibits plant growth. How this process is prevented to ensure proper plant growth has not been determined. Here, we report that Arabidopsis S-HsfA2, S-HsfA4c, and S-HsfB1 confer extreme heat (45°C) sensitivity and represent new kinds of HSF with a unique truncated DNA-binding domain (tDBD) that binds a new heat-regulated element (HRE). The HRE conferred a minimal promoter response to heat and exhibited heat stress sensing and transmission patterns. We used S-HsfA2 to investigate whether and how S-HSFs prevent hyperactivation of the canonical HSR. HSP17.6B, a direct target gene of HsfA2, conferred thermotolerance, but its overexpression caused HSR hyperactivation. We revealed that S-HsfA2 alleviated this hyperactivation in two different ways. 1) S-HsfA2 negatively regulates HSP17.6B via the HRE-HRE-like element, thus constructing a noncanonical HSR (S-HsfA2-HRE- HSP17.6B ) to antagonistically repress HsfA2-activated HSP17.6B expression. 2) S-HsfA2 binds to the DBD of HsfA2 to prevent HsfA2 from binding to HSEs, eventually attenuating HsfA2-activated HSP17.6B promoter activity. Overall, our findings underscore the biological importance of S-HSFs, namely, preventing plant heat tolerance hyperactivation to maintain proper growth.

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### Competing Interest Statement

The authors have declared no competing interest.

 [1]: pending:yes

Short heat shock factor A2 confers heat sensitivity in Arabidopsis: Insights into heat resistance and growth balance

短熱休克因子a2在阿拉伯芥中導致熱敏感性-洞見熱抗性和生長平衡


短熱休克因子A2在阿拉伯芥中導致熱敏感性:洞見熱抗性和生長平衡



睾丸生精細胞在出生後發育過程中經歷了大規模的染色質重塑,部分與基因表達譜和轉錄因子結合位點的富集有關。成年生精細胞中一些特定的染色質可及區域與增強子和啟動子相關的組蛋白修飾有關。一些這些區域與多個轉錄因子結合位點富集和差異表達基因相鄰。


In mammals, spermatogonial cells (SPGs) are undifferentiated male germ cells in testis that are quiescent until birth and then self-renew and differentiate to produce spermatogenic cells and functional sperm from early postnatal life throughout adulthood. The transcriptome of SPGs is highly dynamic and timely regulated during postnatal development. We examined if such dynamics involves changes in chromatin organization by profiling the transcriptome and chromatin accessibility of SPGs from early postnatal stages to adulthood in mice using deep RNA-seq, ATAC-seq and computational deconvolution analyses. By integrating transcriptomic and epigenomic features, we show that SPGs undergo massive chromatin remodeling during postnatal development that partially correlates with distinct gene expression profiles and transcription factors (TF) motif enrichment. We identify genomic regions with significantly different chromatin accessibility in adult SPGs that are marked by histone modifications associated with enhancers and promoters. Some of the regions with increased accessibility correspond to transposable element subtypes enriched in multiple TFs motifs and close to differentially expressed genes. Our results underscore the dynamics of chromatin organization in developing germ cells and complement existing datasets on SPGs by providing maps of the regulatory genome at high resolution from the same cell populations at early postnatal, late postnatal and adult stages collected from single individuals.

### Competing Interest Statement

The authors have declared no competing interest.

Dynamics of transcriptional programs and chromatin accessibility in mouse spermatogonial cells from early postnatal to adult life

成年和幼年睾丸生精細胞的轉錄組和表觀基因組特徵揭示了睾丸發育過程中不同的染色質調控景觀


小鼠精子鉤在雌性生殖道中的遷移過程中扮演關鍵角色,提供機械支撐並促進精子與雌性生殖道上皮的相互作用。


In most murine species, spermatozoa exhibit a falciform apical hook at the head end. The function of the sperm hook is not yet clearly understood. In this study, we investigate the role of the sperm hook in the migration of spermatozoa through the female reproductive tract in Mus musculus (C57BL/6), using a deep tissue imaging custom-built two-photon microscope. Through live reproductive tract imaging, we found evidence indicating that the sperm hook aids in the attachment of spermatozoa to the epithelium and facilitates interactions between spermatozoa and the epithelium during migration in the uterus and oviduct. We also observed synchronised sperm beating, which resulted from the spontaneous unidirectional rearrangement of spermatozoa in the uterus. Based on live imaging of spermatozoa-epithelium interaction dynamics, we propose that the sperm hook plays a crucial role in successful migration through the female reproductive tract by providing anchor-like mechanical support and facilitating interactions between spermatozoa and the female reproductive tract in the house mouse.

### Competing Interest Statement

The authors have declared no competing interest.

The sperm hook in house mice: a functional adaptation for migration and self-organised behaviour

雄性小鼠的精子鉤-在雌性生殖道中的遷移和自組織行為的功能性適應


雄性小鼠的精子鉤:在雌性生殖道中的遷移和自組織行為的功能性適應



一個微RNA簇miR-277/34調控了昆蟲變態過程中的性別差異,通過調控與雄性激素和脫皮激素相關的基因通路。


Insects comprise the majority of all described animal species and dominate the terrestrial habitats. The evolution of insect metamorphosis played a profound role in their successful adaptation and radiation. Insect metamorphosis is dependent on hormones ecdysteroids and sesquiterpenoids such as juvenile hormone. Despite the fact there are genuine differences between sexes during insect metamorphosis which facilitate their successful mating, how such sexual dimorphism in metamorphosis is being controlled is poorly known. We first generated transcriptomic profiles of male and female flies in late larvae and early pupae stages. Using a combination of genome-wide prediction and in vitro dual-luciferase validations, members of a microRNA cluster miR-277/34 were found to potentially regulate the neuropeptide receptor ( AstC-R1 ) that when activated inhibits the sesquiterpenoid pathway and a juvenile hormone-dependent transcription factor ( Kr-h1 ) in fly Drosophila melanogaster. Loss-of-function mutants were created deleting either miR-277 or miR-34, and expression levels of both AstC-R1 and Kr-h1 as well as ecdysteroid and sesquiterpenoid hormone titres were altered. Further comparison of transcriptomes of the late larvae and early pupae of both sexes revealed differential gene pathways being regulated by members of miR-277/34 between sexes during metamorphosis. This study highlights how members of a microRNA cluster control hormonal and developmental gene pathways in different sexes of insects during metamorphosis.

### Competing Interest Statement

The authors have declared no competing interest.

Insect metamorphosis is regulated differently between sexes by members of a microRNA cluster

不同性別的昆蟲變態過程由一個微rna簇調控


不同性別的昆蟲變態過程由一個微RNA簇調控



在哺乳類配子受精後,H3K4me2在前植入期發育過程中經歷了大規模的重塑。


Upon sperm and oocyte fertilization, drastic histone modification reprograming occurs during preimplantation development. However, the global H3K4me2 landscape and its dynamics reprogramming in this period remains largely unknown. Herein we investigate the erasure and re-establishment of H3K4me2 in mouse GV, MII and embryos using an improved approach called Cleavage Under Targets and Release Using Nuclease (CUT&RUN) for histone modification with high-throughput sequencing. We find H3K4me2 extensively exists as a non-canonical pattern in mouse GV oocytes and early embryos. Interestingly, H3K4me2 is erased in MII oocyte and re-established in late 2-cell stage. Importantly, mouse embryos acquire widespread H3K4me2 in CpG-rich and hypomethylated regulatory regions in 4-cell stage, as well as 8-cell stage, but drastic changes happen upon ICM, these CpG-rich H3K4me2 regulatory regions then resolve to either active or repressed states. In summary, our study not only unveil that H3K4me2 transition from parental to zygote, but also provide a H3K4me2 profile during early embryo development, and this will enhance our comprehension to epigenetic reprogramming during mouse early development and in vitro fertilization.

Highlight 

1.  H3K4me2 present differential patterns in sperm and oocytes, as no-canonical pattern in GV oocytes but canonical of sperm in mouse.

2.  GV H3K4me2 peaks were almost erased in MII oocytes, and reconstructed accompanying ZGA occurred, the first landscape of H3K4me2 during early mammalian development was provided.

3.  Non-canonical H3K4me2 in mammalian embryos and pervasive H3K4me2 in CpG-rich regulatory regions in 4 and 8-cell embryos.

4.  CpG-rich H3K4me2 regulatory regions resolve to either active or repressed states in ICM.

### Competing Interest Statement

The authors have declared no competing interest.

Resetting of H3K4me2 during mammalian parental-to-zygote transition

重塑哺乳類父母到合子過渡期的h3k4me2


重塑哺乳類父母到合子過渡期的H3K4me2
