David C. Page

Last updated
David Page
Born
David C. Page

1956 (age 66–67)
Harrisburg, Pennsylvania
NationalityAmerican
Alma mater
Awards
Scientific career
Fields Genetics
Institutions
Doctoral students Bruce Lahn
Website wi.mit.edu/people/faculty/page

David C. Page (born 1956) is an American biologist and professor at the Massachusetts Institute of Technology (MIT), the director of the Whitehead Institute, and a Howard Hughes Medical Institute (HHMI) investigator. [2] He is best known for his work on mapping the Y-chromosome and on its evolution in mammals and expression during development. He was cited by Bryan Sykes in Adam's Curse: A Future Without Men. [3]

Contents

Education and early life

Page was born in Harrisburg, Pennsylvania, in 1956 and grew up in the rural outskirts of Pennsylvania Dutch country. [1] [4] [5] The first of his family to go to college, Page attended Swarthmore College, where he graduated with a BA with highest honors in chemistry in 1978. [4] [6] During his final year at Swarthmore, Page attended class just one day a week and spent the rest of his time researching chromatin structure in the laboratory of molecular biologist Robert Simpson at the National Institutes of Health. [4] [6] In 1978, Page enrolled at Harvard Medical School and the Harvard-MIT Health Sciences Program, where he worked in the laboratories of David Botstein at MIT and Raymond White at the University of Massachusetts Medical School. [6] In White's lab, Page worked on a project to develop a genetic linkage map of the human genome that would become a precursor to the Human Genome Project. [1] The work relied on locating restriction fragment length polymorphisms (RFLP). The first RFLP that Page found was from a site of homology between the X chromosome and Y chromosome, a coincidence that would set the direction of his subsequent career. [1]

Page finished his MD degree in the spring of 1984 and started his own lab as the first Whitehead Fellow at the Whitehead Institute for Biomedical Research researching the genetics of XX male syndrome, or de la Chapelle Syndrome. [1] [6] After Page won the MacArthur "Genius Grant" in 1986, Page was promoted to the faculty of the Whitehead Institute and the MIT Department of Biology in 1988. [6] [7] In 1990, Page was named a Howard Hughes Medical Institute Investigator, and in 2005 he was named as director of the Whitehead Institute. [6]

Research and career

Page has worked in several areas of genetics. [8] [9]

Mapping the Y chromosome

In his work on de la Chapelle Syndrome in 1986, Page collaborated with the geneticist who originally identified the first XX male, Albert de la Chapelle, and geneticist Jean Weissenbach to show that XX males carry a small piece of the Y chromosome. [1] [10] [11]

In the following year, he reported that the gene ZFY induced the development of the testes, a finding which received a great deal of media attention since it putatively resolving a decade-long search for the sex-determining gene. [1] [12] In 1989, a British team of scientists led by Peter Goodfellow and Robin Lovell-Badge began to report that the testis-determining gene was not ZFY, which led Page to review his data. Page found that he had misinterpreted his data because one of the XY females in his study had a second deletion at the site which proved to be the location of the real sex-determining gene. Launching a second round of media attention, Nature published his findings together with a paper from the British group that identified the sex-determining gene, which they termed SRY. [1] [12] [13]

Despite a belief among geneticists that the Y chromosome contained few genes other than the sex-determining gene, Page continued to map the Y chromosome. He had already published DNA-based deletion maps of the Y chromosome in 1986, [14] and went on to develop comprehensive clone-based physical maps of the chromosome in 1992 [15] [16] and systematic catalogs of Y-linked genes in 1997. [17] Page collaborated with a team at the Genome Institute at Washington University to make a complete map of the Y chromosome, which they achieved in 2003. [18] To do so, Page and his colleagues developed a new sequencing technique, single-haplotype iterative mapping and sequencing (SHIMS), since mammalian sex chromosomes contain too many repetitive sequences to be sequenced by conventional approaches. [4] The development of SHIMS allowed Page to identify long palindromic sequences on the long arm of the Y chromosome, which he would go on to show made the Y chromosome vulnerable to the deletions that cause spermatogenic failure (an inability to produce sperm). [19] In 2012, Page characterized the most common genetic cause of spermatogenic failure, the deletion of the AZFc region of the Y chromosome. [20] [21] The lab also found that aberrant crossing over within the Y chromosome's palindromes underlies a wide range of disorders of sexual differentiation, including Turner syndrome. [20]

Evolution of the Y chromosome

With the development of more detailed maps of the Y chromosome, in the mid-1990s Page began to find genetic evidence confirming the theory that both the X and Y chromosomes had evolved from autosomes, beginning with the 1996 discovery that a family of genes called DAZ (deleted in azoospermia) had been transposed from an autosome to the Y chromosome. [4] [22] In 1999, Page and his then-graduate student Bruce Lahn showed that the X and Y chromosomes had diverged in four steps, beginning 200-300 million years ago. [23] Later cross-species comparisons would show that while ancestral genes on the Y chromosome initially underwent rapid decay, [18] [24] the remaining genes have remained stable for the last 25 million years, [25] overturning the long-held view that the Y chromosome was going extinct. [4] In a 2014 study, Page concluded that the conserved genes on the Y chromosome played an important role in male viability, since they were dosage-dependent genes with similar but not identical counterparts on the X chromosome that all have regulatory roles in transcription, translation, and protein stability. Because these genes are expressed throughout the body, Page further concluded that these genes give rise to differences in the biochemistry of male and female tissues. [26]

In super-resolution studies of the sex chromosomes, Page has found evidence of an evolutionary "arms race" between the X and Y chromosomes for transmission to the next generation. In one study, Page found that human X and mouse Y chromosomes have converged, independently acquiring and amplifying gene families expressed in testicular germ cells. [27] Another study found that the mouse Y chromosome had acquired and massively amplified genes homologous to the testis-expressed gene families on the mouse X chromosome. [28]

The genetics of germ cells

Page used the mouse as a model to study the genetics of meiotic initiation, showing that retinoic acid (RA) is the key factor which induces meiosis, as well as identifying several important genes crucial to the meiotic initiation pathway, including Stra8 and DAZL. [29] [30] [31] Page further discovered that the differentiation germ cells into gametocytes (oocytes in females or spermatocytes in males) does not depend on meiotic initiation, as commonly thought, showing that germ cells deficient in Stra8, a gene that activates the meiotic pathway, are still capable of growth and differentiation. [32] [33]

Awards and honors

His honors and awards include:

Related Research Articles

<span class="mw-page-title-main">Meiosis</span> Cell division producing haploid gametes

Meiosis is a special type of cell division of germ cells in sexually-reproducing organisms that produces the gametes, such as sperm or egg cells. It involves two rounds of division that ultimately result in four cells with only one copy of each chromosome (haploid). Additionally, prior to the division, genetic material from the paternal and maternal copies of each chromosome is crossed over, creating new combinations of code on each chromosome. Later on, during fertilisation, the haploid cells produced by meiosis from a male and a female will fuse to create a cell with two copies of each chromosome again, the zygote.

<span class="mw-page-title-main">Y chromosome</span> Sex chromosome in the XY sex-determination system

The Y chromosome is one of two sex chromosomes in therian mammals and other organisms. The other sex chromosome is the X chromosome. Y is normally the sex-determining chromosome in many species, since it is the presence or absence of Y that determines the male or female sex of offspring produced in sexual reproduction. In mammals, the Y chromosome contains the gene SRY, which triggers development of male gonads. The DNA in the human Y chromosome is composed of about 62 million base pairs, making it similar in size to chromosome 19. Genes of the Y chromosome is passed only from male parents to male offsprings over generations. With a 30% difference between humans and chimpanzees, the Y chromosome is one of the fastest-evolving parts of the human genome. The human Y chromosome carries 693 genes, with 107 of these being protein-coding, but some genes are repeated and that makes the number of exclusive protein-coding genes just 42, the numbers are given for telomere-to-telomere CHM13. The Consensus Coding Sequence (CCDS) Project only classified 63 out of 107. All single-copy Y-linked genes are hemizygous except in cases of aneuploidy such as XYY syndrome or XXYY syndrome. Because of fake gaps inserted in GRCh38 it may be not obvious that CHM13 added 30 million base pairs into the Y chromosome, which is almost half of it that was unknown before 2022. In 2023 it was discovered Y chromosome can vary in size a lot: 45.2 million to 84.9 million.

<span class="mw-page-title-main">Germline mutation</span> Inherited genetic variation

A germline mutation, or germinal mutation, is any detectable variation within germ cells. Mutations in these cells are the only mutations that can be passed on to offspring, when either a mutated sperm or oocyte come together to form a zygote. After this fertilization event occurs, germ cells divide rapidly to produce all of the cells in the body, causing this mutation to be present in every somatic and germline cell in the offspring; this is also known as a constitutional mutation. Germline mutation is distinct from somatic mutation.

<span class="mw-page-title-main">X-inactivation</span> Inactivation of copies of X chromosome

X-inactivation is a process by which one of the copies of the X chromosome is inactivated in therian female mammals. The inactive X chromosome is silenced by being packaged into a transcriptionally inactive structure called heterochromatin. As nearly all female mammals have two X chromosomes, X-inactivation prevents them from having twice as many X chromosome gene products as males, who only possess a single copy of the X chromosome.

Meiotic drive is a type of intragenomic conflict, whereby one or more loci within a genome will affect a manipulation of the meiotic process in such a way as to favor the transmission of one or more alleles over another, regardless of its phenotypic expression. More simply, meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time. According to Buckler et al., "Meiotic drive is the subversion of meiosis so that particular genes are preferentially transmitted to the progeny. Meiotic drive generally causes the preferential segregation of small regions of the genome".

The short-stature homeobox gene (SHOX), also known as short-stature-homeobox-containing gene, is a gene located on both the X and Y chromosomes, which is associated with short stature in humans if mutated or present in only one copy (haploinsufficiency).

A chromosomal abnormality, chromosomal anomaly, chromosomal aberration, chromosomal mutation, or chromosomal disorder, is a missing, extra, or irregular portion of chromosomal DNA. These can occur in the form of numerical abnormalities, where there is an atypical number of chromosomes, or as structural abnormalities, where one or more individual chromosomes are altered. Chromosome mutation was formerly used in a strict sense to mean a change in a chromosomal segment, involving more than one gene. Chromosome anomalies usually occur when there is an error in cell division following meiosis or mitosis. Chromosome abnormalities may be detected or confirmed by comparing an individual's karyotype, or full set of chromosomes, to a typical karyotype for the species via genetic testing.

<span class="mw-page-title-main">DAZL</span> Protein-coding gene in the species Homo sapiens

Deleted in azoospermia-like is a protein that in humans is encoded by the DAZL gene.

<span class="mw-page-title-main">DAZ1</span> Protein-coding gene in the species Homo sapiens

Deleted in azoospermia 1, also known as DAZ1, is a protein which in humans is encoded by the DAZ1 gene.

<span class="mw-page-title-main">USP9Y</span> Protein-coding gene in the species Homo sapiens

Ubiquitin specific peptidase 9, Y-linked , also known as USP9Y, is an enzyme which in humans is encoded by the USP9Y gene. It is required for sperm production. This enzyme is a member of the peptidase C19 family and is similar to ubiquitin-specific proteases, which cleave the ubiquitin moiety from ubiquitin-fused precursors and ubiquitinylated proteins.

<span class="mw-page-title-main">DAZ3</span> Protein-coding gene in the species Homo sapiens

Deleted in azoospermia protein 3 is a protein that in humans is encoded by the DAZ3 gene.

<span class="mw-page-title-main">DAZ2</span> Protein-coding gene in the species Homo sapiens

Deleted in azoospermia protein 2 is a protein that in humans is encoded by the DAZ2 gene.

<span class="mw-page-title-main">ZFY</span> Protein-coding gene in the species Homo sapiens

Zinc finger Y-chromosomal protein is a protein that in humans is encoded by the ZFY gene of the Y chromosome.

<span class="mw-page-title-main">DMRT1</span> Protein-coding gene in humans

Doublesex and mab-3 related transcription factor 1, also known as DMRT1, is a protein which in humans is encoded by the DMRT1 gene.

<span class="mw-page-title-main">BOLL</span> Protein-coding gene in the species Homo sapiens

Protein boule-like is a protein that in humans is encoded by the BOLL gene.

<span class="mw-page-title-main">UTY (gene)</span> Protein-coding gene in the species Homo sapiens

Histone demethylase UTY is an enzyme that in humans is encoded by the UTY gene.

<span class="mw-page-title-main">EIF1AY</span> Protein-coding gene in the species Homo sapiens

Eukaryotic translation initiation factor 1A, Y-chromosomal is a protein that in humans is encoded by the EIF1AY gene.

<span class="mw-page-title-main">PRDM9</span> Protein-coding gene in humans

PR domain zinc finger protein 9 is a protein that in humans is encoded by the PRDM9 gene. PRDM9 is responsible for positioning recombination hotspots during meiosis by binding a DNA sequence motif encoded in its zinc finger domain. PRDM9 is the only speciation gene found so far in mammals, and is one of the fastest evolving genes in the genome.

<span class="mw-page-title-main">STAG3 (gene)</span> Protein-coding gene in the species Homo sapiens

Stromal antigen 3 is a protein that in humans is encoded by the STAG3 gene. STAG3 protein is a component of a cohesin complex that regulates the separation of sister chromatids specifically during meiosis. STAG3 appears to be paramount in sister-chromatid cohesion throughout the meiotic process in human oocytes and spermatocytes.

X chromosome reactivation (XCR) is the process by which the inactive X chromosome (the Xi) is re-activated in the cells of eutherian female mammals. Therian female mammalian cells have two X chromosomes, while males have only one, requiring X-chromosome inactivation (XCI) for sex-chromosome dosage compensation. In eutherians, XCI is the random inactivation of one of the X chromosomes, silencing its expression. Much of the scientific knowledge currently known about XCR comes from research limited to mouse models or stem cells.

References

  1. 1 2 3 4 5 6 7 8 9 Trivedi, Bijal (2006). "Profile of David C. Page". Proceedings of the National Academy of Sciences of the United States of America. 103 (8): 2471–2473. Bibcode:2006PNAS..103.2471T. doi: 10.1073/pnas.0600615103 . ISSN   0027-8424. PMC   1413862 . PMID   16481618.
  2. ↑ "David C. Page". HHMI.org.
  3. ↑ Sykes, Bryan (2004). Adam's curse : a future without men (1st ed.). New York: W.W. Norton. ISBN   0393058964. OCLC   54487538.
  4. 1 2 3 4 5 6 "Why, Oh Y? | The Scientist Magazine". The Scientist. Retrieved 2016-02-04.
  5. ↑ Jagetia, Riya; Berg, Elizabeth; Kim, Jae Hyun; Jones, Brianna (Spring 2015). "MURJ Spotlight: Professor David C. Page, Director of the Whitehead Institute" (PDF). MIT Undergraduate Research Journal. Archived from the original (PDF) on 23 February 2016. Retrieved 4 February 2016.
  6. 1 2 3 4 5 6 7 "DAVID PAGE LABORATORY". pagelab.wi.mit.edu. Retrieved 2016-02-04.
  7. ↑ Cruzan Morton, Carol (September 1999). "Save the males: David Page '78 reveals the evolutionary roots of sex and gender" (PDF). Swarthmore Bulletin. Retrieved 4 February 2016.
  8. ↑ David C. Page publications indexed by Google Scholar OOjs UI icon edit-ltr-progressive.svg
  9. ↑ Wade, Nicholas (September 14, 2009). "New Clues to Sex Anomalies in How Y Chromosomes Are Copied". The New York Times– via NYTimes.com.
  10. ↑ Page, D. C.; de la Chapelle, A.; Weissenbach, J. (1985-05-16). "Chromosome Y-specific DNA in related human XX males". Nature. 315 (6016): 224–226. Bibcode:1985Natur.315..224P. doi:10.1038/315224a0. ISSN   0028-0836. PMID   2987697. S2CID   4344130.
  11. ↑ Andersson, M.; Page, D. C.; de la Chapelle, A. (1986-08-15). "Chromosome Y-specific DNA is transferred to the short arm of X chromosome in human XX males". Science. 233 (4765): 786–788. Bibcode:1986Sci...233..786A. doi:10.1126/science.3738510. ISSN   0036-8075. PMID   3738510. S2CID   32456133.
  12. 1 2 Page, D. C.; Mosher, R.; Simpson, E. M.; Fisher, E. M.; Mardon, G.; Pollack, J.; McGillivray, B.; de la Chapelle, A.; Brown, L. G. (1987-12-24). "The sex-determining region of the human Y chromosome encodes a finger protein". Cell. 51 (6): 1091–1104. doi:10.1016/0092-8674(87)90595-2. ISSN   0092-8674. PMID   3690661. S2CID   7454260.
  13. ↑ Sinclair, A. H.; Berta, P.; Palmer, M. S.; Hawkins, J. R.; Griffiths, B. L.; Smith, M. J.; Foster, J. W.; Frischauf, A. M.; Lovell-Badge, R. (1990-07-19). "A gene from the human sex-determining region encodes a protein with homology to a conserved DNA-binding motif". Nature. 346 (6281): 240–244. Bibcode:1990Natur.346..240S. doi:10.1038/346240a0. ISSN   0028-0836. PMID   1695712. S2CID   4364032.
  14. ↑ Vergnaud, G; Page, D C; Simmler, M C; Brown, L; Rouyer, F; Noel, B; Botstein, D; de la Chapelle, A; Weissenbach, J (1986-02-01). "A deletion map of the human Y chromosome based on DNA hybridization". American Journal of Human Genetics. 38 (2): 109–124. ISSN   0002-9297. PMC   1684749 . PMID   3004206.
  15. ↑ Vollrath, Douglas; Foote, Simon; Hilton, Adrienne; Brown, Laura G.; Beer-Romero, Peggy; Bogan, Jonathan; Page, David C. (2 October 1992). "The Human Y Chromosome: A 43-Interval Map Based on Naturally Occurring Deletions" (PDF). Science. 258 (5079): 52–59. Bibcode:1992Sci...258...52V. doi:10.1126/science.1439769. PMID   1439769 . Retrieved 4 February 2016.
  16. ↑ Foote, Simon; Vollrath, Douglas; Hilton, Adrienne; Page, David C. (2 October 1992). "The Human Y Chromosome: Spanning the Euchromatic Region" (PDF). Science. 258 (5079): 60–66. doi:10.1126/science.1359640. PMID   1359640 . Retrieved 4 February 2016.
  17. ↑ Lahn, Bruce; Page, David C. (24 October 1997). "Functional Coherence of the Human Y Chromosome" (PDF). Science. 278 (5338): 675–680. Bibcode:1997Sci...278..675L. doi:10.1126/science.278.5338.675. PMID   9381176 . Retrieved 4 February 2016.
  18. 1 2 Skaletsky, H.; Kuroda-Kawaguchi, T.; Minx, P. J.; Cordum, H. S.; Hillier, L.; Brown, L. G.; Repping, S.; Pyntikova, T.; Ali, J.; Bieri, T.; Chinwalla, A.; Delehaunty, A.; Delehaunty, K.; Du, H.; Fewell, G.; Fulton, L.; Fulton, R.; Graves, T.; Hou, S. F.; Latrielle, P.; Leonard, S.; Mardis, E.; Maupin, R.; McPherson, J.; Miner, T.; Nash, W.; Nguyen, C.; Ozersky, P.; Pepin, K.; Rock, S. (2003). "The male-specific region of the human Y chromosome is a mosaic of discrete sequence classes". Nature. 423 (6942): 825–837. Bibcode:2003Natur.423..825S. doi: 10.1038/nature01722 . PMID   12815422.
  19. ↑ Repping, Sjoerd; Skaletsky, Helen; Lange, Julian; Silber, Sherman; Van Der Veen, Fulco; Oates, Robert D.; Page, David C.; Rozen, Steve (2002-10-01). "Recombination between palindromes P5 and P1 on the human Y chromosome causes massive deletions and spermatogenic failure". American Journal of Human Genetics. 71 (4): 906–922. doi:10.1086/342928. ISSN   0002-9297. PMC   419997 . PMID   12297986.
  20. 1 2 "Whitehead Institute - Faculty". wi.mit.edu.
  21. ↑ Rozen, Steven G.; Marszalek, Janet D.; Irenze, Kathryn; Skaletsky, Helen; Brown, Laura G.; Oates, Robert D.; Silber, Sherman J.; Ardlie, Kristin; Page, David C. (2012-11-02). "AZFc deletions and spermatogenic failure: a population-based survey of 20,000 Y chromosomes". American Journal of Human Genetics. 91 (5): 890–896. doi:10.1016/j.ajhg.2012.09.003. ISSN   1537-6605. PMC   3487143 . PMID   23103232.
  22. ↑ Saxena, R.; Brown, L. G.; Hawkins, T.; Alagappan, R. K.; Skaletsky, H.; Reeve, M. P.; Reijo, R.; Rozen, S.; Dinulos, M. B. (1996-11-01). "The DAZ gene cluster on the human Y chromosome arose from an autosomal gene that was transposed, repeatedly amplified and pruned". Nature Genetics. 14 (3): 292–299. doi:10.1038/ng1196-292. ISSN   1061-4036. PMID   8896558. S2CID   34964224.
  23. ↑ Lahn, B. T.; Page, D. C. (1999-10-29). "Four evolutionary strata on the human X chromosome". Science. 286 (5441): 964–967. doi:10.1126/science.286.5441.964. ISSN   0036-8075. PMID   10542153.
  24. ↑ Bellott, Daniel W.; Skaletsky, Helen; Pyntikova, Tatyana; Mardis, Elaine R.; Graves, Tina; Kremitzki, Colin; Brown, Laura G.; Rozen, Steve; Warren, Wesley C. (2010-07-29). "Convergent evolution of chicken Z and human X chromosomes by expansion and gene acquisition" (PDF). Nature. 466 (7306): 612–616. Bibcode:2010Natur.466..612B. doi:10.1038/nature09172. ISSN   1476-4687. PMC   2943333 . PMID   20622855.
  25. ↑ Hughes, Jennifer F.; Skaletsky, Helen; Brown, Laura G.; Pyntikova, Tatyana; Graves, Tina; Fulton, Robert S.; Dugan, Shannon; Ding, Yan; Buhay, Christian J. (2012-03-01). "Strict evolutionary conservation followed rapid gene loss on human and rhesus Y chromosomes". Nature. 483 (7387): 82–86. Bibcode:2012Natur.483...82H. doi:10.1038/nature10843. ISSN   0028-0836. PMC   3292678 . PMID   22367542.
  26. ↑ Bellott, Daniel W.; Hughes, Jennifer F.; Skaletsky, Helen; Brown, Laura G.; Pyntikova, Tatyana; Cho, Ting-Jan; Koutseva, Natalia; Zaghlul, Sara; Graves, Tina (2014-04-24). "Mammalian Y chromosomes retain widely expressed dosage-sensitive regulators". Nature. 508 (7497): 494–499. Bibcode:2014Natur.508..494B. doi:10.1038/nature13206. ISSN   0028-0836. PMC   4139287 . PMID   24759411.
  27. ↑ Mueller, Jacob L.; Skaletsky, Helen; Brown, Laura G.; Zaghlul, Sara; Rock, Susan; Graves, Tina; Auger, Katherine; Warren, Wesley C.; Wilson, Richard K. (2013-09-01). "Independent specialization of the human and mouse X chromosomes for the male germ line". Nature Genetics. 45 (9): 1083–1087. doi:10.1038/ng.2705. ISSN   1061-4036. PMC   3758364 . PMID   23872635.
  28. ↑ Soh, Y. Q. Shirleen; Alföldi, Jessica; Pyntikova, Tatyana; Brown, Laura G.; Graves, Tina; Minx, Patrick J.; Fulton, Robert S.; Kremitzki, Colin; Koutseva, Natalia (2014-11-06). "Sequencing the mouse Y chromosome reveals convergent gene acquisition and amplification on both sex chromosomes". Cell. 159 (4): 800–813. doi:10.1016/j.cell.2014.09.052. ISSN   1097-4172. PMC   4260969 . PMID   25417157.
  29. ↑ Baltus, Andrew E.; Menke, Douglas B.; Hu, Yueh-Chiang; Goodheart, Mary L.; Carpenter, Anne E.; de Rooij, Dirk G.; Page, David C. (2006-12-01). "In germ cells of mouse embryonic ovaries, the decision to enter meiosis precedes premeiotic DNA replication". Nature Genetics. 38 (12): 1430–1434. doi:10.1038/ng1919. ISSN   1061-4036. PMID   17115059. S2CID   17258424.
  30. ↑ Lin, Yanfeng; Gill, Mark E.; Koubova, Jana; Page, David C. (2008-12-12). "Germ Cell-Intrinsic and -Extrinsic Factors Govern Meiotic Initiation in Mouse Embryos". Science. 322 (5908): 1685–1687. Bibcode:2008Sci...322.1685L. doi:10.1126/science.1166340. ISSN   0036-8075. PMID   19074348. S2CID   11261341.
  31. ↑ Koubova, Jana; Menke, Douglas B.; Zhou, Qing; Capel, Blanche; Griswold, Michael D.; Page, David C. (2006-02-21). "Retinoic acid regulates sex-specific timing of meiotic initiation in mice". Proceedings of the National Academy of Sciences of the United States of America. 103 (8): 2474–2479. Bibcode:2006PNAS..103.2474K. doi: 10.1073/pnas.0510813103 . ISSN   0027-8424. PMC   1413806 . PMID   16461896.
  32. ↑ Endo, Tsutomu; Romer, Katherine A.; Anderson, Ericka L.; Baltus, Andrew E.; de Rooij, Dirk G.; Page, David C. (2015-05-05). "Periodic retinoic acid-STRA8 signaling intersects with periodic germ-cell competencies to regulate spermatogenesis". Proceedings of the National Academy of Sciences of the United States of America. 112 (18): E2347–2356. Bibcode:2015PNAS..112E2347E. doi: 10.1073/pnas.1505683112 . ISSN   1091-6490. PMC   4426408 . PMID   25902548.
  33. ↑ Dokshin, Gregoriy A.; Baltus, Andrew E.; Eppig, John J.; Page, David C. (2013-08-01). "Oocyte differentiation is genetically dissociable from meiosis in mice". Nature Genetics. 45 (8): 877–883. doi:10.1038/ng.2672. ISSN   1061-4036. PMC   3747777 . PMID   23770609.
  34. ↑ "David C. Page — MacArthur Foundation". www.macfound.org. Retrieved 2016-02-04.
  35. ↑ "Searle Scholars Program : David C. Page (1989)". www.searlescholars.net. Retrieved 2016-02-04.
  36. ↑ Page, David C. (2004-03-01). "On Low Expectations Exceeded; or, The Genomic Salvation of the Y Chromosome". American Journal of Human Genetics. 74 (3): 399–402. doi:10.1086/382659. ISSN   0002-9297. PMC   1182254 . PMID   15053010.
  37. ↑ "MIT Office of the Provost, Institutional Research". web.mit.edu. Retrieved 2016-02-04.
  38. ↑ "Press Releases - American Academy of Arts & Sciences". www.amacad.org. Retrieved 2016-02-04.
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