Editing Maternal effect (section)

==In genetics==

In [[genetics]], a maternal effect occurs when the phenotype of an organism is determined by the genotype of its mother.<ref>{{Cite book | vauthors = Griffiths AJ | title=An Introduction to genetic analysis | year=1999 | publisher=W. H. Freeman | location=New York  | isbn=978-0-7167-3771-1 | url=https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=maternal,effect&rid=iga.section.3739#3740}}{{page needed|date=November 2015}}</ref> For example, if a mutation is maternal effect [[recessive]], then a female homozygous for the mutation may appear phenotypically normal, however her offspring will show the mutant phenotype, even if they are heterozygous for the mutation.
{| class="wikitable" border="1" style="width: 75%; margin: 1em auto 1em auto; background: white;"
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! colspan="4"|Maternal effect
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|style="padding: 1em; background-color: honeydew"|[[File:Maternal effect crosses1.svg|center]]
|style="padding: 1em; background-color: honeydew"|[[File:Maternal effect crosses2.svg|center]]
|style="padding: 1em; background-color: ivory"|[[File:Maternal effect crosses3.svg|center]]
|style="padding: 1em; background-color: ivory"|[[File:Maternal effect crosses4.svg|center]]
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! colspan="2"|All offspring show the wild-type phenotype
! colspan="2"|All offspring show the mutant phenotype
|-
|+ style="caption-side: bottom; font-weight: normal; margin-top: 1em;"|Genetic crosses involving a maternal effect recessive mutation, ''m''. The maternal genotype determines the phenotype of the offspring.
|}
Maternal effects often occur because the mother supplies a particular [[mRNA]] or [[protein]] to the oocyte, hence the maternal genome determines whether the molecule is functional. Maternal supply of mRNAs to the early embryo is important, as in many organisms the embryo is initially transcriptionally inactive.<ref>{{cite journal |author=Schier AF |title=The maternal-zygotic transition: death and birth of RNAs |journal=Science |volume=316 |issue=5823 |pages=406–7 |date=April 2007 |pmid=17446392 |doi=10.1126/science.1140693 |bibcode=2007Sci...316..406S|s2cid=36999389 }}</ref> Because of the inheritance pattern of maternal effect mutations, special [[genetic screen]]s are required to identify them. These typically involve examining the phenotype of the organisms one generation later than in a conventional ([[zygote|zygotic]]) screen, as their mothers will be potentially homozygous for maternal effect mutations that arise.<ref>{{cite journal |vauthors=Jorgensen EM, Mango SE |title=The art and design of genetic screens: ''Caenorhabditis elegans'' |journal=Nat. Rev. Genet. |volume=3 |issue=5 |pages=356–69 |date=May 2002 |pmid=11988761 |doi=10.1038/nrg794 |s2cid=152517 }}</ref><ref>{{cite journal |author=St Johnston D |title=The art and design of genetic screens: ''Drosophila melanogaster'' |journal=Nat. Rev. Genet. |volume=3 |issue=3 |pages=176–88 |date=March 2002 |pmid=11972155 |doi=10.1038/nrg751 |s2cid=6093235 }}</ref>

===In ''Drosophila'' early embryogenesis===
[[File:Ribonucleoprotein particles in the Drosophila egg chamber.png|thumb|right|Protein and RNA are transported in particles (white dots) from the nurse cells (maternal) to the developing oocyte in ''Drosophila melanogaster''. Scale bar shows 10&nbsp;μm.]]
{{further|Drosophila embryogenesis}}

A ''[[Drosophila melanogaster]]'' [[oocyte]] develops in an egg chamber in close association with a set of cells called [[nurse cell]]s. Both the oocyte and the nurse cells are descended from a single germline [[stem cell]], however [[cytokinesis]] is incomplete in these [[cell division]]s, and the cytoplasm of the nurse cells and the oocyte is connected by structures known as [[ring canal]]s.<ref>{{cite journal |vauthors=Bastock R, St Johnston D |title=''Drosophila'' oogenesis |journal=Curr. Biol. |volume=18 |issue=23 |pages=R1082–7 |date=December 2008 |pmid=19081037 |doi=10.1016/j.cub.2008.09.011 |s2cid=14924601 |doi-access=free |bibcode=2008CBio...18R1082B }}</ref> Only the oocyte undergoes [[meiosis]] and contributes [[DNA]] to the next generation.

Many maternal effect ''Drosophila'' mutants have been found that affect the early steps in embryogenesis such as [[axis determination]], including ''[[bicoid]], [[dorsal (gene)|dorsal]], [[gurken]]'' and ''[[oskar (gene)|oskar]]''.<ref>{{cite journal |vauthors=Nüsslein-Volhard C, Lohs-Schardin M, Sander K, Cremer C |title=A dorso-ventral shift of embryonic primordia in a new maternal-effect mutant of ''Drosophila'' |journal=Nature |volume=283 |issue=5746 |pages=474–6 |date=January 1980 |pmid=6766208 |doi= 10.1038/283474a0|bibcode = 1980Natur.283..474N |s2cid=4320963 }}</ref><ref>{{cite journal |vauthors=Schüpbach T, Wieschaus E |title=Germline autonomy of maternal-effect mutations altering the embryonic body pattern of ''Drosophila'' |journal=Dev. Biol. |volume=113 |issue=2 |pages=443–8 |date=February 1986 |pmid=3081391 |doi= 10.1016/0012-1606(86)90179-X}}</ref><ref>{{cite journal |vauthors=Nüsslein-Volhard C, Frohnhöfer HG, Lehmann R |title=Determination of anteroposterior polarity in ''Drosophila'' |journal=Science |volume=238 |issue=4834 |pages=1675–81 |date=December 1987 |pmid=3686007 |doi= 10.1126/science.3686007|bibcode = 1987Sci...238.1675N }}</ref> For example, embryos from homozygous ''bicoid'' mothers fail to produce head and [[thorax]] structures.

Once the gene that is disrupted in the ''bicoid'' mutant was identified, it was shown that ''bicoid'' mRNA is [[Transcription (genetics)|transcribed]] in the nurse cells and then relocalized to the oocyte.<ref>{{cite journal  |vauthors=Berleth T, Burri M, Thoma G, etal |title=The role of localization of ''bicoid'' RNA in organizing the anterior pattern of the ''Drosophila'' embryo |journal=EMBO J. |volume=7 |issue=6 |pages=1749–56 |date=June 1988 |pmid=2901954 |pmc=457163 |doi= 10.1002/j.1460-2075.1988.tb03004.x}}</ref> Other maternal effect mutants either affect products that are similarly produced in the nurse cells and act in the oocyte, or parts of the transportation machinery that are required for this relocalization.<ref>{{cite journal |vauthors=Ephrussi A, St Johnston D |title=Seeing is believing: the Bicoid morphogen gradient matures |journal=Cell |volume=116 |issue=2 |pages=143–52 |date=January 2004 |pmid=14744427 |doi= 10.1016/S0092-8674(04)00037-6|s2cid=1977542 |doi-access=free }}</ref> Since these genes are expressed in the (maternal) nurse cells and not in the oocyte or fertilised embryo, the maternal genotype determines whether they can function.

'''Maternal effect genes'''<ref>{{Cite book|title=Life Sciences : Fundamentals and practice.| last1 = Pranav | first1 = Kumar | last2 = Mina | first2 = Usha | name-list-style = vanc |date=2013|publisher=Pathfinder Academy |isbn=9788190642774 |edition=3rd |location=New Delhi |oclc=857764171 }}</ref> are expressed during oogenesis by the mother (expressed prior to fertilization) and develop the anterior-posterior and dorsal ventral polarity of the egg. The anterior end of the egg becomes the head; posterior end becomes the tail. the dorsal side is on the top; the ventral side is in underneath. The products of maternal effect genes called maternal mRNAs are produced by nurse cell and follicle cells and deposited in the egg cells (oocytes). At the start of development process, mRNA gradients are formed in oocytes along anterior-posterior and dorsal ventral axes.

About thirty maternal genes are involved in pattern formation have been identified. In particular, products of four maternal effect genes are critical to the formation of anterior-posterior axis. The product of two maternal effect gene, bicoid and hunchback, regulates formation of anterior structure while another pair nanos and caudal, specifies protein that regulates formation of posterior part of embryo.

The transcript of all four genes-bicoid, hunchback, caudal, nanos are synthesized by nurse and follicle cells and transported into the oocytes.

===In birds===
In birds, mothers may pass down hormones in their eggs that affect an offspring's growth and behavior. Experiments in [[domestic canaries]] have shown that eggs that contain more yolk androgens develop into chicks that display more social dominance. Similar variation in yolk androgen levels has been seen in bird species like the [[American coot#Maternal effects|American coot]], though the mechanism of effect has yet to be established.<ref>{{cite journal | vauthors = Reed WL, Clark ME | title = Beyond maternal effects in birds: responses of the embryo to the environment | journal = Integrative and Comparative Biology | volume = 51 | issue = 1 | pages = 73–80 | date = July 2011 | pmid = 21624931 | doi = 10.1093/icb/icr032 | doi-access = free }}</ref>

=== In humans ===
In 2015, obesity theorist Edward Archer published "The Childhood Obesity Epidemic as a Result of Nongenetic Evolution: The Maternal Resources Hypothesis" and a series of works on maternal effects in human [[obesity]] and health.<ref>{{cite journal | vauthors = Archer E | title = The childhood obesity epidemic as a result of nongenetic evolution: the maternal resources hypothesis | language = en | journal = Mayo Clinic Proceedings | volume = 90 | issue = 1 | pages = 77–92 | date = January 2015 | pmid = 25440888 | pmc = 4289440 | doi = 10.1016/j.mayocp.2014.08.006 | url = http://www.mayoclinicproceedings.org/article/S0025-6196%252814%252900740-X/fulltext }}</ref><ref>{{cite journal | vauthors = Archer E | title = In reply—Maternal, paternal, and societal efforts are needed to "cure" childhood obesity | language = en | journal = Mayo Clinic Proceedings | volume = 90 | issue = 4 | pages = 555–7 | date = April 2015 | pmid = 25841259 | pmc = 4527549 | doi = 10.1016/j.mayocp.2015.01.020 | url = http://www.mayoclinicproceedings.org/article/S0025-6196%252815%252900121-4/fulltext }}</ref><ref>{{cite journal | vauthors = Archer E | title = In reply--Epigenetics and Childhood Obesity | language = en | journal = Mayo Clinic Proceedings | volume = 90 | issue = 5 | pages = 693–5 | date = May 2015 | pmid = 25939942 | doi = 10.1016/j.mayocp.2015.02.013 | url = http://www.mayoclinicproceedings.org/article/S0025-6196%252815%252900186-X/fulltext | doi-access = free }}</ref><ref>{{cite journal |last=Archer |first=Edward | name-list-style = vanc |date=2015-02-28 |title=The mother of all problems|journal=New Scientist|volume=225|issue=3010|pages=32–33|doi=10.1016/S0262-4079(15)60404-3|bibcode=2015NewSc.225...32A}}</ref> In this body of work, Archer argued that accumulative maternal effects via the non-genetic evolution of matrilineal nutrient metabolism is responsible for the increased global prevalence of obesity and [[diabetes mellitus type 2]]. Archer posited that decrements in maternal metabolic control altered fetal pancreatic [[beta cell]], [[adipocyte]] (fat cell) and [[myocyte]] (muscle cell) development thereby inducing an enduring competitive advantage of adipocytes in the acquisition and sequestering on nutrient energy.

===In plants===
The environmental cues such as light, temperature, soil moisture and nutrients that the mother plant encounters can cause variations in seed quality, even within the same genotype. Thus, the mother plant greatly influences seed traits such as seed size, germination rate, and viability.<ref>{{cite journal | vauthors = Nguyen, Chi D | title = Effects of Maternal Environment on Seed Germination and Seedling Vigor of Petunia x Hybrida under Different Abiotic Stresses | journal =  Plants | volume = 10 | issue = 3 | pages = 581 | date = March 2021 | doi =10.3390/plants10030581| pmid = 33808598 | pmc = 8003445 | doi-access = free }}</ref>