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#gene expression

168 public questions tagged with this topic.

Xenopus nodal-related (Xnr) gene expression is activated by:

Vegetal T-box factor VegT induces Nodal-related genes in vegetal endoderm via Smad-activated enhancers, while nuclear beta-catenin on dorsal side binds TCF to activate Siamois. Siamois and VegT cooperatively bind Xnr enhancers, synergistically upregulating Xnr1,2,5,6 on dorsal side highest, ventral side moderate, establishing gradient. BMP and Activin also modulate but transcriptional activation fundamentally requires both beta-catenin dorsal cue and VegT mesendoderm competence factor. Double knockdown eliminates mesoderm entirely. Thus intersection explains dorsal-high Nodal gradient establishing organizer position and patterning mesoderm along dorsoventral axis.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Xnr activation by beta-catenin and VegT co-regulation.

Injection of antisense Wnt11 oligonucleotides results in:

Maternally encoded Wnt11 ligand normally activates canonical Wnt pathway vegetally, stabilizing beta-catenin dorsally via Dishevelled and GBP inhibiting GSK-3. Injecting antisense Wnt11 morpholino oligonucleotides depletes ligand, preventing Dishevelled activation, leaving GSK-3 active throughout embryo, causing beta-catenin degradation ubiquitously. Consequently Siamois and Xnr genes not transcribed in Nieuwkoop center, dorsal mesoderm absent, organizer fails, embryo becomes ventralized with excess blood and epidermis lacking notochord and neural plate. Rescue with stabilized beta-catenin mRNA restores organizer and secondary axis, proving Wnt11 upstream required for organizer formation and dorsal axis specification.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Antisense Wnt11 leads to failure of organizer formation.

Activin at high concentration near beads induces expression of:

Animal cap sandwich experiments with Activin-soaked beads reveal concentration-dependent gene activation mirroring in vivo Nodal gradient. Cells directly contacting high dose bead experience maximal Smad2 signaling activating high-threshold genes goosecoid and chordin forming head organizer and prechordal mesoderm marked by Cerberus and Frzb. Slightly distant cells receiving moderate dose activate Xbra and form trunk mesoderm, furthest cells become ventral mesoderm. Therefore high concentration near beads induces goosecoid expression defining dorsalmost axial mesoderm, analogous to dorsal vegetal cells receiving highest Nodal. This illustrates conserved developmental logic of morphogen gradients patterning embryonic axes through Wnt and BMP antagonism.

Ref: Green and Smith, Activin concentration gradient and Xenopus gene activation, Nature 1990.

Expression of Wnt4 gene primarily promotes:

Wnt4 is secreted glycoprotein of Wnt family functioning as pivotal ovary-determining signal. Expressed in bipotential gonad and upregulated specifically in XX somatic cells, Wnt4 activates canonical β-catenin cascade via Frizzled receptors, leading to stabilization of β-catenin and transcription of Dax1, Fst and Foxl2. This promotes granulosa fate, survival of germ cells entering meiosis, vascular patterning typical of ovary and maintenance of Müllerian ducts. Wnt4 knockout XX mice exhibit partial female-to-male reversal with Wolffian duct persistence, androgen synthesis, oocyte loss and ectopic testis cords, revealing requirement.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 6: Wnt4 in ovary determination and Müllerian duct maintenance.

Alcohol-exposed fetuses have reduced expression of:

Sonic hedgehog morphogen produced by prechordal mesoderm and ventral midline is essential for frontonasal prominence outgrowth and medial facial development. Alcohol consumption during critical gastrulation window impairs cholesterol modification of Shh protein necessary for signaling potency and reduces Shh transcription via oxidative injury to midline cells. Mouse models show ethanol exposure decreases Shh mRNA in frontonasal ectoderm leading to reduced proliferation and increased apoptosis of facial mesenchyme, phenotypes rescued by Shh agonists or cholesterol supplementation. Reduced Shh expression therefore mediates midfacial hypoplasia, holoprosencephaly spectrum features observed in fetal alcohol syndrome pathogenesis.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 20: Alcohol reduces Sonic hedgehog expression.

Which gene is critical for abdominal formation in Drosophila?

Abdominal segmentation outcome depends on posterior morphogen Caudal which activates posterior gap genes. While Bicoid specifies head and Hunchback thoracic domain, Caudal gradient highest posteriorly turns on knirps and giant that pattern abdominal segments A1-A8. In caudal mutants, anterior head and thorax form but abdomen is deleted, replaced by mirrored thorax or ectopic filzkorper loss. Nanos is required to clear Hunchback posteriorly permitting Caudal activity, but Caudal itself is direct transcriptional activator of abdominal fate. Gurken influences dorsoventral polarity. Hence Caudal is critical determinant for abdominal formation and posterior patterning execution.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Caudal function in abdominal patterning.

Posterior organizing center defined by:

Posterior organizing center established by localization of nanos mRNA to posterior pole plasm via actin and oskar-dependent anchoring. Translation of Nanos in posterior blastoderm represses hunchback via Pumilio, permitting posterior gap gene expression and abdomen formation. Simultaneously Nanos specifies pole cells germline precursors. Gurken marks dorsal follicle side, Bicoid anterior, Dorsal ventral embryonic nuclei; none define posterior center. Nanos mutation eliminates abdominal segments producing head thorax only. Nanos gradient therefore provides second axis information complementary to anterior Bicoid morphogen gradient during blastoderm patterning and germline specification.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Nanos defines posterior organizing center - repression of hunchback translation.

Parasegments differ from segments because:

Parasegments are functional genetic units defined by expression borders of pair-rule and segment polarity genes, notably engrailed stripes labeling anterior boundary of parasegment, whereas segments are morphological constrictions visible later through cuticular grooves offset posteriorly by half unit. Parasegment boundaries coincide with lineage restriction compartments maintained by lineage rather than grooves. Therefore parasegments represent genetic domains where regulatory interactions maintain identity, while segments reflect morphological boundaries. This distinction explains why wingless and engrailed interact across parasegment border but later furrow lies behind engrailed stripe.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Parasegment versus segment - genetic domains offset by lineage compartments.

Expression of pair-rule genes occurs in:

After gap proteins establish regional information, pair-rule genes including even-skipped, fushi tarazu, hairy, runt translate graded inputs into periodic expression via combinatorial enhancer logic integrating Bicoid activation and Gap repression. At syncytial blastoderm each gene resolves into seven transverse stripes encircling embryo, corresponding to alternate parasegments. Uniform bands represent maternal genes, posterior domain gap genes. Seven-stripe configuration provides first metameric prepattern visualized by antibody staining, serving as landmarks that activate segment polarity genes in fourteen stripes, converting double-segment periodicity into single-segment repeat during germband extension and patterning.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Pair-rule genes - seven alternating stripes at blastoderm stage.

MP and NPH4 promote expression of:

MP/ARF5 and NPH4/ARF7 auxin response factors become transcriptionally active when auxin triggers TIR1/AFB-mediated ubiquitination and proteasomal degradation of BODENLOS and other AUX/IAA repressors containing EAR motifs. Activated ARFs bind canonical auxin response elements TGTCTC in promoters of PLETHORA genes particularly PLT1, PLT2, PLT4/BABYBOOM, PLT5/AIL5 rapidly inducing their expression in basal and root pole during embryogenesis. MP-PLT module directly converts auxin accumulation into root stem cell specification program, stabilizing PIN expression creating self-reinforcing auxin-PLT-PIN loop crucial for embryonic root establishment and post-embryonic maintenance.

Ref: Berleth & Jürgens, Development 1993: MP and NPH4/ARF7 promote PLT expression establishing root fate downstream of auxin.

Organizing center expresses:

Organizing center in shoot apical meristem is small group of cells at base of central zone directly beneath totipotent stem cells functioning as niche organizer analogous to animal stem cell niches. It uniquely expresses WUSCHEL transcription factor whose protein migrates via plasmodesmata to overlying central zone conferring stem cell identity and activating CLV3 peptide expression. WUS expression is positively regulated by cytokinin via ARR, HAM GRAS factors, and low auxin, and negatively by CLV signaling through feedback loop. Thus organizing center serves as signaling source orchestrating meristem homeostasis and size maintenance.

Ref: Laux et al., Development 1996; Mayer et al.: Organizing center expresses WUSCHEL transcription factor in SAM.

STM gene maintains:

SHOOT MERISTEMLESS encodes KNOX1 class homeobox protein expressed throughout shoot apical meristem dome but sharply downregulated in incipient leaf primordia by ASYMMETRIC LEAVES1/2 repression pathway. STM prevents premature differentiation by promoting cytokinin biosynthesis through IPT7 activation, repressing gibberellin 20-oxidase genes maintaining low active GA, repressing CUC boundary regulators at proper domains, and protecting stem cell identity. Strong stm mutants fail to establish embryonic SAM, exhibit fused cotyledons, lack vegetative growth, arrest as seedlings, demonstrating absolute requirement for maintaining shoot meristem identity and indeterminate self-renewal capacity.

Ref: Long & Barton, Development 1998; Laux et al.: STM maintains shoot meristem identity and indeterminate growth, KNOX.