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The zinc-finger protein Zelda is a key activator of the early zygotic genome in Drosophila.

Liang HL, Nien CY, Liu HY, Metzstein MM, Kirov N, Rushlow C - Nature (2008)

Bottom Line: However, the transcription factor(s) that activate the zygotic genome remain elusive.Mutant embryos lacking zld are defective in cellular blastoderm formation, and fail to activate many genes essential for cellularization, sex determination and pattern formation.Global expression profiling confirmed that Zld has an important role in the activation of the early zygotic genome and suggests that Zld may also regulate maternal RNA degradation during the maternal-to-zygotic transition.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, New York University, 100 Washington Square East, New York, New York 10003, USA.

ABSTRACT
In all animals, the initial events of embryogenesis are controlled by maternal gene products that are deposited into the developing oocyte. At some point after fertilization, control of embryogenesis is transferred to the zygotic genome in a process called the maternal-to-zygotic transition. During this time, many maternal RNAs are degraded and transcription of zygotic RNAs ensues. There is a long-standing question as to which factors regulate these events. The recent findings that microRNAs and Smaug mediate maternal transcript degradation have shed new light on this aspect of the problem. However, the transcription factor(s) that activate the zygotic genome remain elusive. The discovery that many of the early transcribed genes in Drosophila share a cis-regulatory heptamer motif, CAGGTAG and related sequences, collectively referred to as TAGteam sites raised the possibility that a dedicated transcription factor could interact with these sites to activate transcription. Here we report that the zinc-finger protein Zelda (Zld; Zinc-finger early Drosophila activator) binds specifically to these sites and is capable of activating transcription in transient transfection assays. Mutant embryos lacking zld are defective in cellular blastoderm formation, and fail to activate many genes essential for cellularization, sex determination and pattern formation. Global expression profiling confirmed that Zld has an important role in the activation of the early zygotic genome and suggests that Zld may also regulate maternal RNA degradation during the maternal-to-zygotic transition.

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Maternal zld transcripts are lost as zygotic zld is activated in cycle 14Wild-type (wt; a-d) and zld294 (e-j) ovaries (a) and embryos (b-j) were hybridized with zld (all but g) or bcd (g) RNA probes. (a) mid (left) and late-stage (right) egg chambers with zld transcripts in the nurse cells (nc) but not the columnar follicle cells that overlay the oocyte. (b) Unfertilized egg. (c) cycle 14 embryo undergoing cellularization. (d) late-stage embryo. (e) M+Z- zld cycle 14 embryo. Maternal zld transcripts have disappeared. (f) M- zld cycle 10-11 embryo. (g) M- zld cycle 14 embryo has a normal bcd pattern. (h) M-Z- zld late cycle14 embryo showing anomalous distribution of cytoplasm (arrows). (i) M-Z+ zld early cycle 14 embryo showing onset of zygotic zld expression. (j) M-Z+ zld late cycle14 embryo showing abnormalities (arrows).
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Figure 2: Maternal zld transcripts are lost as zygotic zld is activated in cycle 14Wild-type (wt; a-d) and zld294 (e-j) ovaries (a) and embryos (b-j) were hybridized with zld (all but g) or bcd (g) RNA probes. (a) mid (left) and late-stage (right) egg chambers with zld transcripts in the nurse cells (nc) but not the columnar follicle cells that overlay the oocyte. (b) Unfertilized egg. (c) cycle 14 embryo undergoing cellularization. (d) late-stage embryo. (e) M+Z- zld cycle 14 embryo. Maternal zld transcripts have disappeared. (f) M- zld cycle 10-11 embryo. (g) M- zld cycle 14 embryo has a normal bcd pattern. (h) M-Z- zld late cycle14 embryo showing anomalous distribution of cytoplasm (arrows). (i) M-Z+ zld early cycle 14 embryo showing onset of zygotic zld expression. (j) M-Z+ zld late cycle14 embryo showing abnormalities (arrows).

Mentions: zld transcripts were detected in the germline cells of the ovary (Fig. 2a), in unfertilized eggs (Fig. 2b), and throughout early development (Fig. 2c). Later zld becomes restricted to the nervous system and specific head regions (Fig. 2d), as previously shown10. To analyze zld function, we generated deletion alleles of zld by imprecise excision (schematized in Fig. 1b). Hemizygous embryos showed abnormal CNS and head development (data not shown), consistent with previous reports of CG12701 lethal P-insertion phenotypes10,11. zld transcripts were not observed in these embryos after cycle 14 (Fig. 2e). However, younger embryos had high levels of maternal zld transcripts (data not shown), indicating that maternally loaded zld transcripts are degraded during cellularization, and replaced with zygotic zld.


The zinc-finger protein Zelda is a key activator of the early zygotic genome in Drosophila.

Liang HL, Nien CY, Liu HY, Metzstein MM, Kirov N, Rushlow C - Nature (2008)

Maternal zld transcripts are lost as zygotic zld is activated in cycle 14Wild-type (wt; a-d) and zld294 (e-j) ovaries (a) and embryos (b-j) were hybridized with zld (all but g) or bcd (g) RNA probes. (a) mid (left) and late-stage (right) egg chambers with zld transcripts in the nurse cells (nc) but not the columnar follicle cells that overlay the oocyte. (b) Unfertilized egg. (c) cycle 14 embryo undergoing cellularization. (d) late-stage embryo. (e) M+Z- zld cycle 14 embryo. Maternal zld transcripts have disappeared. (f) M- zld cycle 10-11 embryo. (g) M- zld cycle 14 embryo has a normal bcd pattern. (h) M-Z- zld late cycle14 embryo showing anomalous distribution of cytoplasm (arrows). (i) M-Z+ zld early cycle 14 embryo showing onset of zygotic zld expression. (j) M-Z+ zld late cycle14 embryo showing abnormalities (arrows).
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Related In: Results  -  Collection

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Figure 2: Maternal zld transcripts are lost as zygotic zld is activated in cycle 14Wild-type (wt; a-d) and zld294 (e-j) ovaries (a) and embryos (b-j) were hybridized with zld (all but g) or bcd (g) RNA probes. (a) mid (left) and late-stage (right) egg chambers with zld transcripts in the nurse cells (nc) but not the columnar follicle cells that overlay the oocyte. (b) Unfertilized egg. (c) cycle 14 embryo undergoing cellularization. (d) late-stage embryo. (e) M+Z- zld cycle 14 embryo. Maternal zld transcripts have disappeared. (f) M- zld cycle 10-11 embryo. (g) M- zld cycle 14 embryo has a normal bcd pattern. (h) M-Z- zld late cycle14 embryo showing anomalous distribution of cytoplasm (arrows). (i) M-Z+ zld early cycle 14 embryo showing onset of zygotic zld expression. (j) M-Z+ zld late cycle14 embryo showing abnormalities (arrows).
Mentions: zld transcripts were detected in the germline cells of the ovary (Fig. 2a), in unfertilized eggs (Fig. 2b), and throughout early development (Fig. 2c). Later zld becomes restricted to the nervous system and specific head regions (Fig. 2d), as previously shown10. To analyze zld function, we generated deletion alleles of zld by imprecise excision (schematized in Fig. 1b). Hemizygous embryos showed abnormal CNS and head development (data not shown), consistent with previous reports of CG12701 lethal P-insertion phenotypes10,11. zld transcripts were not observed in these embryos after cycle 14 (Fig. 2e). However, younger embryos had high levels of maternal zld transcripts (data not shown), indicating that maternally loaded zld transcripts are degraded during cellularization, and replaced with zygotic zld.

Bottom Line: However, the transcription factor(s) that activate the zygotic genome remain elusive.Mutant embryos lacking zld are defective in cellular blastoderm formation, and fail to activate many genes essential for cellularization, sex determination and pattern formation.Global expression profiling confirmed that Zld has an important role in the activation of the early zygotic genome and suggests that Zld may also regulate maternal RNA degradation during the maternal-to-zygotic transition.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, New York University, 100 Washington Square East, New York, New York 10003, USA.

ABSTRACT
In all animals, the initial events of embryogenesis are controlled by maternal gene products that are deposited into the developing oocyte. At some point after fertilization, control of embryogenesis is transferred to the zygotic genome in a process called the maternal-to-zygotic transition. During this time, many maternal RNAs are degraded and transcription of zygotic RNAs ensues. There is a long-standing question as to which factors regulate these events. The recent findings that microRNAs and Smaug mediate maternal transcript degradation have shed new light on this aspect of the problem. However, the transcription factor(s) that activate the zygotic genome remain elusive. The discovery that many of the early transcribed genes in Drosophila share a cis-regulatory heptamer motif, CAGGTAG and related sequences, collectively referred to as TAGteam sites raised the possibility that a dedicated transcription factor could interact with these sites to activate transcription. Here we report that the zinc-finger protein Zelda (Zld; Zinc-finger early Drosophila activator) binds specifically to these sites and is capable of activating transcription in transient transfection assays. Mutant embryos lacking zld are defective in cellular blastoderm formation, and fail to activate many genes essential for cellularization, sex determination and pattern formation. Global expression profiling confirmed that Zld has an important role in the activation of the early zygotic genome and suggests that Zld may also regulate maternal RNA degradation during the maternal-to-zygotic transition.

Show MeSH
Related in: MedlinePlus