Qhov sib txawv tseem ceeb ntawm qhov tseem ceeb thiab qhov tsis zoo yog qhov tseem ceeb ntawm epistasis, qhov tseem ceeb ntawm cov noob caj noob ces npog qhov kev qhia ntawm tag nrho cov alleles ntawm lwm cov noob, thaum nyob rau hauv recessive epistasis, recessive alleles ntawm ib lub noob npog qhov kev qhia ntawm tag nrho cov alleles ntawm lwm cov noob.
Epistasis yog ib qho tshwm sim lossis ib hom kev sib cuam tshuam polygenic uas ib tus noob tswj hwm qhov phenotype ntawm lwm cov noob rau qhov zoo. Ob lub noob muaj kev cuam tshuam rau lub cev ntawm qhov zoo, tab sis ib qho uas qhia tias epistasis npog cov nyhuv ntawm lwm tus. Cov noob uas qhia tias epistasis tuaj yeem yog qhov tseem ceeb lossis rov ua dua. Yog li ntawd, qhov tseem ceeb thiab qhov tsis zoo ntawm cov epistasis yog ntau hom epistasis.
Dominant Epistasis yog dab tsi?
Qee zaus, ib qho tseem ceeb ntawm allele ntawm ib qho chaw npog qhov phenotype ntawm qhov chaw thib ob. Qhov no hu ua dominant epistasis. Cov txiv hmab txiv ntoo thiab paj xim ntawm cov nroj tsuag yog ib qho piv txwv uas siv los piav txog qhov tseem ceeb ntawm epistasis. Txiv hmab txiv ntoo xim nyob rau hauv lub caij ntuj sov squash yog qhia nyob rau hauv no txoj kev. Homozygous recessive qhia ntawm W gene (ww) ua ke nrog homozygous dominant lossis heterozygous dominant qhia ntawm Y gene (YY lossis Yy) nyob rau lub caij ntuj sov squash ua cov txiv hmab txiv ntoo daj, thaum wwyy (ob hom noob recessive) genotype tsim cov txiv hmab txiv ntoo ntsuab. Txawm li cas los xij, yog tias daim ntawv theej ntawm W gene muaj nyob rau hauv homozygous lossis heterozygous daim ntawv, lub caij ntuj sov squash yuav yog cov txiv hmab txiv ntoo dawb tsis hais txog Y alleles.
Nyob hauv sorghum, cov nplej yog pearly los yog chalky. Thaum cov nroj tsuag nrog pearly nplej thiab lwm yam nrog chalky nplej hla, qhov tshwm sim F1 pejxeem yog pearly. F2 pejxeem cais qauv yog 3 pearly: 1 chalky. Ib yam li ntawd, cov xim nplej yog xim liab lossis dawb. Thaum cov nroj tsuag nrog cov nplej liab thiab lwm yam nrog cov nplej dawb hla, cov neeg F1 tshwm sim liab. Thiab F2 pej xeem sib cais qauv yog 3 liab: 1 dawb. Cov xim liab ntawm cov nplej npog qhov kev qhia ntawm lwm tus cwj pwm; nws yog pearliness los yog chalkiness ntawm grain. Thaum cov nplej xim dawb, nws muaj peev xwm hais tias cov nplej yog pearly lossis chalky. Tab sis thaum cov nplej liab, nws tsis tuaj yeem hais tias cov nplej yog pearly lossis chalky. Qhov sib piv F2 classical ntawm 9: 3: 3: 1 hloov pauv mus rau 12: 3: 1 hauv qhov tseem ceeb epistasis.
Daim duab 01: Epistasis
Tsis muaj ib qho piv txwv yooj yim ntawm cov kab mob tseem ceeb hauv tib neeg. Txawm li cas los xij, cov kws tshawb fawb ntseeg tias qhov no yog ib qho ntawm cov txheej txheem uas cuam tshuam nrog cov kab mob nyuaj xws li Alzheimer's disease, autism, thiab ntshav qab zib.
YDab tsi yog Recessive Epistasis?
Nyob rau hauv cov kab mob tsis zoo, cov kab mob tsis zoo ntawm ib lub noob npog qhov phenotypic qhia ntawm cov noob thib ob. Hauv lwm lo lus, thaum ib lub noob yog homozygous recessive, nws zais qhov phenotype ntawm lwm tus. Ib qho piv txwv paub zoo ntawm kev rov ua kom rov zoo li qub yog pigmentation hauv nas. Lub tsho tiv no tsiaj qus, agouti (AA) yog qhov tseem ceeb rau cov xim plaub (aa). Txawm li cas los xij, cais cov noob (C) yog qhov tsim nyog rau kev tsim cov pigmentation.
Ib tus nas uas muaj c allele ntawm qhov chaw no tsis tuaj yeem tsim cov xim thiab yog albino txawm hais tias cov allele tam sim no nyob rau hauv locus A. Yog li ntawd, cov genotypes AAcc, Aacc, thiab aacc txhua tus tsim muaj albino phenotype. Hauv qhov no, C gene yog epistatic rau A gene. Cov classical F2 kev sib cais ntawm 9: 3: 3: 1 tau hloov pauv mus rau 9: 3: 4 hauv kev rov ua dua tshiab.
Dab tsi yog qhov zoo sib xws ntawm Dominant thiab Recessive Epistasis?
- Lawv yog kev sib txuas ntawm caj ces.
- Lawv yog ob hom epistasis.
- Nyob rau hauv ob qho xwm txheej, alleles ntawm ib lub noob npog lub phenotype ntawm alleles ntawm lwm cov noob.
- Lawv tseem ceeb heev rau kev qhia txog noob caj noob ces thiab ntau hom caj ces.
Qhov txawv ntawm Dominant thiab Recessive Epistasis yog dab tsi?
Cov noob ntawm ib tug neeg tsis qhia tawm ntawm ib leeg; Hloov chaw, lawv ua haujlwm hauv ib puag ncig zoo. Yog li ntawd, kev sib cuam tshuam ntawm cov noob tshwm sim. Kev sib cuam tshuam ntawm cov noob yog antagonistic hauv epistasis, ib lub noob npog qhov kev qhia ntawm lwm tus. Hauv qhov tseem ceeb ntawm epistasis, qhov tseem ceeb ntawm ib lub noob npog qhov kev qhia ntawm tag nrho cov alleles ntawm lwm cov noob, whereas, nyob rau hauv recessive epistasis, lub recessive alleles ntawm ib tug noob npog qhov kev qhia ntawm tag nrho cov alleles ntawm lwm cov noob. Yog li, qhov no yog qhov sib txawv tseem ceeb ntawm qhov tseem ceeb thiab kev rov ua dua tshiab.
Cov hauv qab no infographic tabulates qhov sib txawv ntawm qhov tseem ceeb thiab qhov rov ua dua rau kev sib piv ntawm ib sab.
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Qhov sib txawv ntawm Dominant thiab Recessive Epistasis hauv Tabular Form
Summary – Dominant vs Recessive Epistasis
Epistasis tuaj yeem txhais tau tias yog kev sib cuam tshuam ntawm cov noob uas ib tus noob cuam tshuam nrog cov phenotypic qhia ntawm lwm cov noob uas tsis yog allelic. Cov noob uas npog qhov phenotypic qhia ntawm lwm cov noob uas tsis yog-allelic yog hu ua epistatic gene. Cov noob uas raug txwv los ntawm cov noob epistatic hu ua hypostatic gene. Muaj ntau hom epistasis ua qhov tseem ceeb thiab rov ua dua. Epistatic gene yog nyob rau hauv lub xeev tseem ceeb nyob rau hauv dominant epistasis thaum epistatic noob nyob rau hauv lub xeev recessive nyob rau hauv recessive epistasis. Yog li, qhov no yog cov ntsiab lus ntawm qhov sib txawv ntawm qhov tseem ceeb thiab qhov rov ua dua tshiab.
