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#mammals

42 public questions tagged with this topic.

Developmental biology Basics

Genomic equivalence in mammals was first demonstrated by:

While Briggs and King showed frog nuclei retained developmental potency in amphibians, mammalian genomic equivalence required additional technical advances due to small eggs and implantation requirements. Ian Wilmut and colleagues at Roslin Institute provided definitive mammalian proof by creating Dolly from adult mammary cell nucleus. Surrogate mother carried embryo to term, and microsatellite analysis confirmed genetic identity to donor, not egg donor. Earlier claims by Illmensee and Hoppe about mouse cloning proved irreproducible. Therefore mammalian equivalence first convincingly demonstrated by Wilmut, extending Gurdon's amphibian principle to endothermic vertebrates with placental development.

Ref: Wilmut et al., Nature 1997; Gilbert, 12th ed., Chapter 3: Mammalian genomic equivalence.

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Regeneration -lll

Regeneration of mammalian hair follicles exemplifies:

Mammalian hair follicle exemplifies stem-cell mediated regeneration where dedicated resident stem cells fuel cyclical turnover rather than forming blastema or using compensatory division of differentiated cells. Bulge region harbors slow-cycling multipotent stem cells activated by dermal papilla Wnt signals at anagen, producing transient amplifying progeny differentiating into hair lineage. Inhibitory BMP maintains quiescence during telogen. After wounding, bulge cells migrate to epidermis contributing to repair. This paradigm illustrates niche-regulated stem population sustaining tissue renewal, distinguishing stem-cell mediated regeneration from epimorphosis and morphallaxis and highlighting mammalian regenerative strategy for continuously renewing epithelia.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 21: Hair follicle example of stem-cell mediated regeneration.

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Sex determination-l

Mammalian bipotential gonads initially derive from:

Mammalian bipotential gonads arise from intermediate mesoderm forming urogenital ridge flanking dorsal mesentery and coelomic epithelium. Coelomic cells proliferate and ingress into underlying mesenchyme expressing Wt1, Sf1 and Lhx9 contributing supporting precursors, while primordial germ cells migrate from yolk sac endoderm into gonadal anlage. Hence gonad classified as mesodermal organ sharing lineage with kidneys and adrenal cortex, not ectodermal or neural crest derived. Mesodermal origin provides stromal, steroidogenic and supporting lineages later differentiating into granulosa or Sertoli cells under sex-determining signals and hormones.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 6: Bipotential gonads from intermediate mesoderm.

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Sex determination-l

Leydig cells in mammals produce:

Leydig cells originate from mesenchymal progenitors in interstitial compartment under Desert hedgehog signaling from Sertoli cells and transcription factor Sf1. They express steroidogenic acute regulatory protein and enzymes Cyp11a1, Hsd3b1, Cyp17a1 converting cholesterol to testosterone. Their principal product testosterone secreted in fetal life stabilizes Wolffian ducts differentiating into seminal vesicles, epididymis and vas deferens, supports masculinization of brain and later promotes spermatogenesis. Testosterone also serves as precursor for dihydrotestosterone in external genitalia and estradiol in brain. Insufficient function causes female phenotype.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 17: Leydig cells produce testosterone in fetal testis.

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Sex determination-l

The primary sex determination in mammals refers to the development of:

Primary sex determination describes initial decision within bipotential gonad whether to become testis or ovary, distinct from secondary sexual characteristics. Process occurs around seventh week in humans when Sry in XY gonads commits supporting lineage to Sertoli fate through Sox9 upregulation and ovary pathway via Wnt4/β-catenin in XX, shaping gonadal architecture. Gonad then secretes hormones Anti-Müllerian hormone and testosterone or estrogen orchestrating secondary determination of internal ducts, external genitalia, brain and general habitus. Primary event therefore corresponds to gonads differentiating into testes or ovaries.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 6: Primary sex determination as gonad fate decision.

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Sex determination-l

Which transcription factor is activated by the SRY gene in mammals?

Sry encodes HMG-domain architectural transcription factor that does not itself complete Sertoli differentiation but initiates cascade by binding Sox9 testis-specific enhancer TESCO cooperatively with Sf1/Nr5a1. Protein induces DNA bending facilitating recruitment of coactivators, chromatin remodeling and sustained Sox9 transcription sufficient to commit supporting lineage. Sox9 fulfills most male functions including Fgf9, Amh induction and cord formation. Therefore immediate direct transcriptional target downstream of Sry is Sox9, functioning as hub for testis program. Other factors like Wnt4 and Foxl2 belong to opposing pathway suppressed.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 6: SRY activates SOX9 as primary target.

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Sex determination-l

In mammals, the presence of the Y chromosome leads to the development of:

Mammalian Y chromosome harbors Sry gene considered testis-determining factor. Presence of Y means presence of Sry whose timely expression in genital ridge precursors between six to seven weeks upregulates Sox9 in pre-Sertoli cells, activating Fgf9 loop, testis cord formation, anti-Müllerian hormone secretion and testosterone synthesis from Leydig cells. Wolffian ducts thus persist while Müllerian ducts regress, generating male phenotype. Absence leaves ovarian pathway established via Wnt4/Rspo1/β-catenin directing ovary formation. Therefore presence of Y chromosome leads anatomically and molecularly to development of testes in normal mammals.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 6: Y chromosome and SRY in testis determination.

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