Direct Induction of DNA Hypermethylation in Sea Urchin Embryos by Microinjection of 5-Methyl dCTP Stimulates Early Histone Gene Expression and Leads to Developmental Arrest

1993 ◽  
Vol 155 (1) ◽  
pp. 75-86 ◽  
Author(s):  
Jeannie Chen ◽  
Rob Maxson ◽  
Peter A. Jones
Keyword(s):  
Gene Expression ◽  
Sea Urchin ◽  
Histone Gene ◽  
Dna Hypermethylation ◽  
Sea Urchin Embryos ◽  
Developmental Arrest ◽  
Histone Gene Expression ◽  
Direct Induction

scholarly journals Monocistronic transcription is the physiological mechanism of sea urchin embryonic histone gene expression.

1981 ◽  
Vol 1 (7) ◽  
pp. 661-671 ◽  
Author(s):  
A Mauron ◽  
S Levy ◽  
G Childs ◽  
L Kedes
Keyword(s):  
Gene Expression ◽  
Steady State ◽  
Early Development ◽  
Sea Urchin ◽  
Dna Sequences ◽  
Messenger Rna ◽  
Physiological Mechanism ◽  
Histone Gene ◽  
Histone Genes ◽  
Histone Gene Expression

We have examined histone gene expression during the early stages of sea urchin embryogenesis. The five histone genes expressed at that time are contained in tandem repetitive segments. It has been suggested that adjacent coding regions and their intervening spacer sequences are transcribed into large polycistronic messenger ribonucleic acid (RNA) precursors. We have subcloned into pBR322 deoxyribonucleic acid (DNA) sequences mapping either in the coding region, the 5' spacer, or the 3' spacer of the H2B histone gene. These clones were used to produce radioiodinated hybridization probes. We measured the steady-state quantity of H2B messenger RNA as well as spacer-specific RNA in the total RNA from embryos taken at various stages of development from fertilization to hatching of blastulae (0 to 22 h post-fertilization). Small amounts of RNA hybridizing to both spacer probes could be found. However, we show that these RNAs form mismatched hybrids with the spacer DNA and therefore cannot originate from the spacers present in the histone genes. We conclude that there is no detectable transcription of the spacer regions on either side of the H2B histone gene. The detection limit for RNA complementary to the 5' spacer sequence corresponds to a maximum of about three RNA molecules per cell, an amount shown to be far less than the projected steady-state pool size of a putative polycistronic transcript, if such a precursor were to be the obligatory transcript of the histone genes. (This conclusion was derived by using the known rates of production of H2B mRNA throughout early development [R. E. Maxson and F. H. Wilt, Dev. Biol., in press].) The physiologically relevant transcript of the histone genes in early development is therefore monocistronic and probably identical to the messenger RNA itself.

scholarly journals Monocistronic transcription is the physiological mechanism of sea urchin embryonic histone gene expression

1981 ◽  
Vol 1 (7) ◽  
pp. 661-671
Author(s):  
A Mauron ◽  
S Levy ◽  
G Childs ◽  
L Kedes
Keyword(s):  
Gene Expression ◽  
Steady State ◽  
Early Development ◽  
Sea Urchin ◽  
Dna Sequences ◽  
Messenger Rna ◽  
Physiological Mechanism ◽  
Histone Gene ◽  
Histone Genes ◽  
Histone Gene Expression

We have examined histone gene expression during the early stages of sea urchin embryogenesis. The five histone genes expressed at that time are contained in tandem repetitive segments. It has been suggested that adjacent coding regions and their intervening spacer sequences are transcribed into large polycistronic messenger ribonucleic acid (RNA) precursors. We have subcloned into pBR322 deoxyribonucleic acid (DNA) sequences mapping either in the coding region, the 5' spacer, or the 3' spacer of the H2B histone gene. These clones were used to produce radioiodinated hybridization probes. We measured the steady-state quantity of H2B messenger RNA as well as spacer-specific RNA in the total RNA from embryos taken at various stages of development from fertilization to hatching of blastulae (0 to 22 h post-fertilization). Small amounts of RNA hybridizing to both spacer probes could be found. However, we show that these RNAs form mismatched hybrids with the spacer DNA and therefore cannot originate from the spacers present in the histone genes. We conclude that there is no detectable transcription of the spacer regions on either side of the H2B histone gene. The detection limit for RNA complementary to the 5' spacer sequence corresponds to a maximum of about three RNA molecules per cell, an amount shown to be far less than the projected steady-state pool size of a putative polycistronic transcript, if such a precursor were to be the obligatory transcript of the histone genes. (This conclusion was derived by using the known rates of production of H2B mRNA throughout early development [R. E. Maxson and F. H. Wilt, Dev. Biol., in press].) The physiologically relevant transcript of the histone genes in early development is therefore monocistronic and probably identical to the messenger RNA itself.

Sea urchin histone genes: the beginning and end of the message

1984 ◽  
Vol 307 (1132) ◽  
pp. 293-295
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Gene Transcription ◽  
Sea Urchin ◽  
Nuclear Dna ◽  
Gene Clusters ◽  
Histone Gene ◽  
Histone Genes ◽  
Histone Gene Expression ◽  
Histone Gene Transcription

The purpose of studies on the regulation of histone gene expression is to explain, for instance, how histone proteins arise in defined stoichiometric relationships in the chromatin, how transcription of histone genes is regulated in the cell cycle and how during the development of some species, histone variant genes are activated sequentially. The control of histone gene expression has m any interesting facets. One is struck by the major differences in balance and importance of the various regulatory mechanisms as they become apparent from investigations in m any laboratories. For example, in yeast, histone gene transcription is tightly coupled to the cell cycle, and the amounts of histone synthesized are determined largely by regulation of histone m RN A turnover (Hereford & Osley 1981). At the other extreme, there is the example of the maturing frog oöcyte where histone m RN A synthesis is uncoupled from DNA synthesis and yields pools of histone 1000-fold in excess of nuclear DNA mass (reviewed by Woodland 1980). Recent reports suggest that even the details of histone gene transcription may vary during the development of the species. The tandem histone gene clusters of sea urchin (G. Spinelli, unpublished results) and frog oocytes are transcribed polycistronically at least at some stages of their development (J. Gall, personal communication), whereas histone gene clusters of the cleaving sea urchin embryos appear to be transcribed monocistronically (Mauron et al. 1981). Finally, in the early embryo the partitioning of the m RN A between nucleus and cytoplasm may be also a regulative process (DeLeon al. 1983).

scholarly journals ALS-linked FUS mutants affect the localization of U7 snRNP and replication-dependent histone gene expression in human cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ankur Gadgil ◽  
Agnieszka Walczak ◽  
Agata Stępień ◽  
Jonas Mechtersheimer ◽  
Agnes Lumi Nishimura ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Polymerase Ii ◽  
Histone Gene ◽  
Cytoplasmic Inclusions ◽  
Cellular Models ◽  
Histone Gene Expression ◽  
Genes Encoding ◽  
U7 Snrnp ◽  
Processing Event ◽  
Fus Protein

AbstractGenes encoding replication-dependent histones lack introns, and the mRNAs produced are a unique class of RNA polymerase II transcripts in eukaryotic cells that do not end in a polyadenylated tail. Mature mRNAs are thus formed by a single endonucleolytic cleavage that releases the pre-mRNA from the DNA and is the only processing event necessary. U7 snRNP is one of the key factors that determines the cleavage site within the 3ʹUTR of replication-dependent histone pre-mRNAs. We have previously showed that the FUS protein interacts with U7 snRNA/snRNP and regulates the expression of histone genes by stimulating transcription and 3ʹ end maturation. Mutations in the FUS gene first identified in patients with amyotrophic lateral sclerosis (ALS) lead to the accumulation of the FUS protein in cytoplasmic inclusions. Here, we report that mutations in FUS lead to disruption of the transcriptional activity of FUS and mislocalization of U7 snRNA/snRNP in cytoplasmic aggregates in cellular models and primary neurons. As a consequence, decreased transcriptional efficiency and aberrant 3ʹ end processing of histone pre-mRNAs were observed. This study highlights for the first time the deregulation of replication-dependent histone gene expression and its involvement in ALS.

scholarly journals Super resolution light microscopy of the Drosophila Histone Locus Body reveals a core-shell organization associated with expression of replication dependent histone genes

2021 ◽  
pp. mbc.E20-10-0645
Author(s):  
James P. Kemp ◽  
Xiao-Cui Yang ◽  
Zbigniew Dominski ◽  
William F. Marzluff ◽  
Robert J. Duronio
Keyword(s):  
Gene Expression ◽  
Gene Transcription ◽  
Nuclear Body ◽  
Histone Gene ◽  
Core Shell ◽  
Histone Genes ◽  
The Core ◽  
Histone Gene Expression ◽  
Histone Locus ◽  
Histone Gene Transcription

The Histone Locus Body (HLB) is an evolutionarily conserved nuclear body that regulates the transcription and processing of replication-dependent (RD) histone mRNAs, which are the only eukaryotic mRNAs lacking a poly-A tail. Many nuclear bodies contain distinct domains, but how internal organization is related to nuclear body function is not fully understood. Here, we demonstrate using structured illumination microscopy that Drosophila HLBs have a “core-shell” organization in which the internal core contains transcriptionally active RD histone genes. The N-terminus of Mxc, which contains a domain required for Mxc oligomerization, HLB assembly, and RD histone gene expression, is enriched in the HLB core. In contrast, the C-terminus of Mxc is enriched in the HLB outer shell as is FLASH, a component of the active U7 snRNP that co-transcriptionally cleaves RD histone pre-mRNA. Consistent with these results, we show biochemically that FLASH binds directly to the Mxc C-terminal region. In the rapid S-M nuclear cycles of syncytial blastoderm Drosophila embryos, the HLB disassembles at mitosis and reassembles the core-shell arrangement as histone gene transcription is activated immediately after mitosis. Thus, the core-shell organization is coupled to zygotic histone gene transcription, revealing a link between HLB internal organization and RD histone gene expression.

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