is a cleft chin dominant or recessive?  can you inherit it from previous generations or must it be father-son, mother-daughter?
127684
I think that is a dominant trait. No one in my family has a cleft chin but my nephew has a cleft chin like his dad (my brother-in-law).
161174
1st part.... usually dominants are beneficial and more common in the population, but not always.  Huntington's disease which is fatal is dominant.  This has stayed in the population because it usually doesn't make the person sick until they are past child-bearing years.  Polydactyly (6 or more digits) is dominant as is syndactyly (fused digits).  Dwarfism is also dominant.\n2nd part...I don't see why not although I don't know of an example.
15544
I disagree with the one said blue eyes are dominant. Actually the gene of blue eyes is resessive. So if either one parents or grandparents have the gene of brown eyes, their offspring can more chances to get brown eyes than blue. Of couse, blue or brown eyes really depends on the genotype of the parents, not the phynotype. So if and only if both parents have blue eyes, they offspring have 100% chances to get pure blue eyes gene. \n\nSO if your eye color is brown, and your children are blue, that means that you have a blue eye gene, but because it is recessive, thus the phynotype of your eye color is brown. Your children would have 1/2 chance to get either blue or brown eye color in this situation.\n\nThe following link talks about the eye color in detail.
439339
1. heterozygous: Punnett square is Pp x pp\n2. dominant b/c if it was recessive that would be the only type of allele the parents would pass on and all their children would have to be intensely freckled\n3. the Punnett square would be a 4x4 box with the B's and C's independant of each other. so on one side you have BC, Bc, bC, and bc with all of those showing up on the other side as well b/c the female was the same genotype as the male.  Obviously the black color is dominant b'c the male is heterozygous and black so all heterozygous offspring and all homozygous dominant offspring will be black as well.  the question gets a little fuzzy here though, i think you may have left some out b/c we don't know which of the two genes controls color or if they both do how the interaction between them works.  I'd be glad to help further if you have any more information to supply.
24521
Caused by a terminal deletion of the most distal band of the short arm of chromosome 1, monosomy 1p36 is the most commonly observed terminal chromosomal deletion, occurring in approximately 1 in 5,000 births (Shaffer and Lupski 2000; Heilstedt et al. 2003b). As first described by the Shaffer lab in 13 subjects (Shapira et al. 1997), craniofacial characteristics of this contiguous gene deletion syndrome (CGDS)--so-called because it involves the deletion of multiple adjacent genes on the same chromosome arm--include late-closing, large anterior fontanels (membranous intervals at the intersection of the cranial bones at the crown of the skull), brachycephaly (disproportionate shortness of the head), deep-set eyes, flat nasal bridge, asymmetric ears, and pointed chin. Monosomy 1p36 is also associated with mental retardation, developmental delay, hearing impairment, seizures, growth impairment, and heart defects (Shapira et al. 1997; Slavotinek et al. 1999; Heilstedt et al. 2003a). Over 90 subjects with rearrangements of 1p36 have enrolled in our studies, of which 61 were recently published (Heilstedt et al. 2003a). The deletion sizes in the subjects vary considerably (Wu et al. 1999; Heilstedt et al. 2003a); however, there is some uniformity in the origin of the deletions, with over 60% being maternally derived (Wu et al. 1999; Heilstedt et al. 2003a). Candidate genes have been proposed for some of the individual features of monosomy 1p36, including seizures (Heilstedt et al. 2001) and facial clefting anomalies (Colmenares et al. 2002). \n\nThe Shaffer laboratory has recently identified possible mechanisms for the generation and/or stabilization of terminal deletions of 1p (Ballif et al. 2003; Ballif et al. 2004a; Ballif et al. 2004b; Gajecka et al. 2005). In addition, the Shaffer laboratory has recently demonstrated the use of microarrays--a rapid, sensitive, and high-resolution technology for the detection of many chromosomal anomalies--in the detection of deletions of 1p36 (Yu et al. 2003). \n\n\ncheck this article\n\nShapira SK, McCaskill C, Northrup H, Spikes AS, Elder FF, Sutton VR, Korenberg JR, Greenberg F, Shaffer LG (1997) Chromosome 1p36 deletions: the clinical phenotype and molecular characterization of a common newly delineated syndrome. Am J Hum Genet 61:642-650
337683
It is an Autosomal Recessive Pattern, and yes it is genetic. To explain this pattern would be to lenghty here, so I would suggest that you go on-line and look up Progeria or Premature Aging. There is all kinds of information available about it.
532895
To start with, You need more information as to the Parental genotype for each question, \nFor example in question (a) since you have only mentioned full dominance, we can either assume both parents will be A/A x A/A. However this cross is useless because you know there will not be variation in the F1 progeny because both are dominant. thus the ratio is 100% all dominant A/A.\nThe second assumption is to cross a dominant parent A/A with a recessive parent a/a. If that's the case then you choose one gamete from each parent to form the F1 as follow\n\nParental Genotype        A/A    x    a/a\nGametes                          A     x    a\n\nF1                                         A/a\n\nfrom here, if you need to get genotype and phenotype ratio for your F2, you need information as to what kind of cross you want do. You can self the F1 or you can testcross with a recessive parent. In either case the ratio is different\n\nSelf-cross                  A/a    x      A/a\nGametes              1/2 A , 1/2 a    x   1/2 A , 1/2 a\n\nF2  punnet square\n..............1/2  A..........1/2 a\n\n1/2 A......1/4 A/A........1/4 A/a\n\n1/2 a.......1/4 A/a........1/4 a/a\n\nPhenotypic ratio of F2:  1/4 A/A; 2/4 A/a; 1/4 a/a = 1:2:1\nGenotypic ratio of F2:  (1/4 A/A + 2/4 A/a); 1/4 a/a = 3:1\n\n\n\nTest-cross                  A/a    x      a/a\nGametes              1/2 A , 1/2 a    x   1/2 a , 1/2 a\n\nF2  punnet square\n..............1/2  A..........1/2 a\n\n1/2 a......1/4 A/a........1/4 a/a\n\n1/2 a.......1/4 A/a.......1/4 a/a\n\nPhenotypic ratio of F2:  1/2 A/a; 1/2 a/a = 1:1\nGenotypic ratio of F2: same as genotypic ratio\n\nquestion (a) is not formulated in a clear way. for example. question (a) should have mentioned something like this:\n\na) The F2 of monohybrid cross with both parents full dominance, or 1 parent full dominance, 1 parent recessive.\n\nIs hard to work in genetics problems when the problem lacks crucial information. let me know if there is more information that you did not write down on your question.
242179
If your mom is not bald, and her dad is, then if you are a male you have a 50% chance of being bald. It doesn't matter if her mom carried the allele or not IF your mom is not bald, because that means that she must have gotten the non-allele gene from her mom, or she would have both genes with the bald allele, and she would be bald herself. I am assuming you are a male. If you are female, then your dad does matter, your dad being bald and your mom being a carrier allows you a 50% chance of being bald.
555026
T-dominant- means no tay-sachs\nt-recessive- tay sachs\n\nto have Tay Sachs you must have 2 recessive alleles so tt (this is homozygous)\nThe only way the parents could have a child with tay sachs is for both to be heterozygous for tay sachs which means Tt.\n\nYour punnent square would look like this:\n\nMom goes across and dad goes down\n\nMom-T    t\n''''''''''''_________\nD  T  I  TT I  Tt  I\nA---------------------              \nD  t  I  Tt    I  tt    I\n------------------------\n\nTo do a punnent square you write out one parent's alleles across the top and the other along the side.  Then in each box you write the alleles that are mix in each box.  You can see that the parents would produce in the first box TT which means that person is homozygous (both the same) (also since both capitols would never pass on tay sachs).   The second box across Tt which is heterozygous.  We call this person a carrier.  A carrier is someone who does NOT have tay sachs, but can give it to someone else.  The first box in the second row is Tt too.  A carrier as well.  The second box in the second row is tt.  This is homozygous again, but since a lower case t represents tay sachs this person has it.  \nSo there are 4 boxes.  1/4 of the time TT- no tay sachs\n                                     2/4 of the time Tt-carrier but no tay sachs\n                             and  1/4 of the time tt-tay sachs\n\n1 divided by 4 is .25 which is 25%.  \nThese parents have a 25% chance of having another child with Tay sachs.\n\nSorry about the punnent sq. I couldn't get it to draw right.
205669
I don't have it, but I do know that when it is a familial disorder, it virtually always passes from mother to children, as it is a mitochondrial disorder, and all cellular organelles come from the mother's egg (the sperm basically supply just the DNA).  It can occur sporadically.  It is a A3243G mutation in the mitochondrial genetic code.  A good resource for the "technical" information.  http://www.emedicine.com/ped/topic1406.htm
193444
Mom Dd\nDad DD\nkid dd \nthe only what that this is actually possible is Nondisjunction\nboth allels had to come from MOm\nlike in kleinfelters syndrome or Trisomy 21 wich causes downs.
345709
I am 29 years old and I was born with a cleft palate, particularly Pierre Robin Syndrome.  I had a corrective surgery at 10 mos old and a pharyngeal flap reconstr at 12 yrs old. I also had a minor rhinoplasty at 18 yrs old.  As a child I had extensive speech therapy.  All I can say is this, as a consequence of my condition I have mitral valve prolapse and sleep apnea (loud snoring)...but overall I am fine.  I have always worked hard to look good and study hard...and am currently graduating medical school hopefully becoming a reconstructive surgeon! Support your child...every case differs in what sort of medical problems the child has..however, the emotional and psychological damage from being born 'abnormal' that can exist can be a problem...but also varies and if you are a parent...support and love your child...knowing that sky's the limit. My parents loved me and made me feel like a princess growing up...I didn't realize something was wrong until I was about 6 and was going to speech therapy without my friends...the person dealing with any adversity is changed for the better because they overcome challenges and obstacles better than the average person!!
493452
Thyroid conditions run in families.  I know you didn't want me to say that, but ... just think, you inherited the family trait!  Now you REALLY fit into the family.  Welcome!
582361
Your dad carried one recessive gene for green eyes, which his gene for brown eyes was dominant, so he shows that he has brown eyes.  you got one recessive gene from your mother, and the recessive gene from your dad, making you show for recessive, making you have green-blue eyes. the same way worked for your son
613608
If it is inhereted then you need to go see a genetic counsseler. They will trace your family pedegree for the trait and find out if it is dominant or reccesive and the likelyhood of passing it on. But as a fair warning if it is somewhat rare and the effects show in you then it is probably reccesive so you have a 100% chance of passing it on. However if it is reccesive and your partener does not pass it on then it wont effect your kids :) ...\n\nsorry if you already know this, my point is you should se a genetic counseler. They will tell you everything you need to know.
24393
Ok, this sounds like a homework question so I'll give you some pointers.\n\n1) Color blindness (being a sex-linked trait) is recessive.\n2) So, the fact that they have a color blind kid means that the child is pure recessive so the mother must be a carrier.\nBased on this, a recessive father (cc) and a carrier mother (Cc) = work your Punnett square.
120047
Let's assume that "tongue rolling" is a dominant trait (I believe it is), and that it is not sex-linked. Let's call the dominant allele "R" and the recessive allele "r". The female must be rr, because the heterozygous condition, Rr, will yield a person who is able to roll her tongue.\n\nAll offspring will be able to roll their tongues.\n\nHere is the cross:\n\n-----R----R----\nr | Rr -- Rr\n\nr | Rr -- Rr\n\nAs you can see, all F1 offspring will be heterozygous, and will therefore all be able to roll their tongues.\n\nBy the way, Grumpykiwi, it doesn't mean that it isn't dominant. It merely means that your mother was HETEROZYGOUS, rather than homozygous dominant, as was the man in the problem.